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1
Bland, Richard D. "Pathophysiology of Neonatal Lung Injury." International Journal of Technology Assessment in Health Care 7, S1 (January 1991): 56–60. http://dx.doi.org/10.1017/s0266462300012514.
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Respiratory distress in newborn and young infants often develops as a result of acute lung injury, in which disruption of the normal barrier function of the pulmonary endothelium and epithelium causes protein-rich interstitial and alveolar edema. Several conditions may initiate acute lung injury, including aspiration of meconium or gastric contents, bacterial or viral infection, overzealous resuscitation, and birth associated with incomplete lung development that requires ventilatory support with positivepressure mechanical ventilation and high concentrations of inspired oxygen. The latter condition usually occurs after premature birth, but it also may occur as a consequence of impaired fetal lung growth secondary to diaphragmatic hernia or chest compression from lack of liquid in the amniotic cavity. Acute lung injury sometimes progresses to a chronic form of lung disease, which is characterized by edema, fibrosis, airway distortion, and nonuniform inflation of the lungs.
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Sundar, Isaac K., Hongwei Yao, Michael T. Sellix, and Irfan Rahman. "Circadian molecular clock in lung pathophysiology." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 10 (November 15, 2015): L1056—L1075. http://dx.doi.org/10.1152/ajplung.00152.2015.
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Disrupted daily or circadian rhythms of lung function and inflammatory responses are common features of chronic airway diseases. At the molecular level these circadian rhythms depend on the activity of an autoregulatory feedback loop oscillator of clock gene transcription factors, including the BMAL1:CLOCK activator complex and the repressors PERIOD and CRYPTOCHROME. The key nuclear receptors and transcription factors REV-ERBα and RORα regulate Bmal1 expression and provide stability to the oscillator. Circadian clock dysfunction is implicated in both immune and inflammatory responses to environmental, inflammatory, and infectious agents. Molecular clock function is altered by exposomes, tobacco smoke, lipopolysaccharide, hyperoxia, allergens, bleomycin, as well as bacterial and viral infections. The deacetylase Sirtuin 1 (SIRT1) regulates the timing of the clock through acetylation of BMAL1 and PER2 and controls the clock-dependent functions, which can also be affected by environmental stressors. Environmental agents and redox modulation may alter the levels of REV-ERBα and RORα in lung tissue in association with a heightened DNA damage response, cellular senescence, and inflammation. A reciprocal relationship exists between the molecular clock and immune/inflammatory responses in the lungs. Molecular clock function in lung cells may be used as a biomarker of disease severity and exacerbations or for assessing the efficacy of chronotherapy for disease management. Here, we provide a comprehensive overview of clock-controlled cellular and molecular functions in the lungs and highlight the repercussions of clock disruption on the pathophysiology of chronic airway diseases and their exacerbations. Furthermore, we highlight the potential for the molecular clock as a novel chronopharmacological target for the management of lung pathophysiology.
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van Zanden, Judith E., Henri G. D. Leuvenink, Erik A. M. Verschuuren, Michiel E. Erasmus, and Maximilia C. Hottenrott. "A translational rat model for ex vivo lung perfusion of pre-injured lungs after brain death." PLOS ONE 16, no. 12 (December 2, 2021): e0260705. http://dx.doi.org/10.1371/journal.pone.0260705.
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The process of brain death (BD) detrimentally affects donor lung quality. Ex vivo lung perfusion (EVLP) is a technique originally designed to evaluate marginal donor lungs. Nowadays, its potential as a treatment platform to repair damaged donor lungs is increasingly studied in experimental models. Rat models for EVLP have been described in literature before, yet the pathophysiology of BD was not included in these protocols and prolonged perfusion over 3 hours without anti-inflammatory additives was not achieved. We aimed to establish a model for prolonged EVLP of rat lungs from brain-dead donors, to provide a reliable platform for future experimental studies. Rat lungs were randomly assigned to one of four experimental groups (n = 7/group): 1) healthy, directly procured lungs, 2) lungs procured from rats subjected to 3 hours of BD and 1 hour cold storage (CS), 3) healthy, directly procured lungs subjected to 6 hours EVLP and 4), lungs procured from rats subjected to 3 hours of BD, 1 hour CS and 6 hours EVLP. Lungs from brain-dead rats showed deteriorated ventilation parameters and augmented lung damage when compared to healthy controls, in accordance with the pathophysiology of BD. Subsequent ex vivo perfusion for 6 hours was achieved, both for lungs of healthy donor rats as for pre-injured donor lungs from brain-dead rats. The worsened quality of lungs from brain-dead donors was evident during EVLP as well, as corroborated by deteriorated ventilation performance, increased lactate production and augmented inflammatory status during EVLP. In conclusion, we established a stable model for prolonged EVLP of pre-injured lungs from brain-dead donor rats. In this report we describe tips and pitfalls in the establishment of the rat EVLP model, to enhance reproducibility by other researchers.
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Levvey, Bronwyn, Kovi Levin, Miranda Paraskeva, Glen Westall, and Gregory Snell. "Donation after Brain Death versus Donation after Circulatory Death: Lung Donor Management Issues." Seminars in Respiratory and Critical Care Medicine 39, no. 02 (March 26, 2018): 138–47. http://dx.doi.org/10.1055/s-0037-1615820.
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AbstractLung transplantation (LTx) has traditionally been limited by a lack of suitable donor lungs. With the recognition that lungs are more robust than initially thought, the size of the donor pool of available lungs has increased dramatically in the past decade. Donation after brain death (DBD) and donation after circulatory death (DCD) lungs, both ideal and extended are now routinely utilized. DBD lungs can be damaged. There are important differences in the public's understanding, legal and consent processes, intensive care unit strategies, lung pathophysiology, logistics, and potential-to-actual donor conversion rates between DBD and DCD. Notwithstanding, the short- and long-term outcomes of LTx from any of these DBD versus DCD donor scenarios are now similar, robust, and continue to improve. Large audits suggest there remains a large untapped pool of DCD (but not DBD) lungs that may yet further dramatically increase lung transplant numbers. Donor scoring systems that might predict the donor conversion rates and lung quality, the role of ex vivo lung perfusion as an assessment and lung resuscitation tool, as well as the potential of donor lung quality biomarkers all have immense promise for the clinical field.
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Naramala, Srikanth, Sharmi Biswas, Sreedhar Adapa, Vijay Gayam, Romeo C. Castillo, Srinadh Annangi, and Venu Madhav Konala. "Pleomorphic Pulmonary Manifestations of IgG4-Related Disease." Case Reports in Rheumatology 2019 (August 20, 2019): 1–4. http://dx.doi.org/10.1155/2019/7572869.
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Immunoglobulin G4-related disease (IgG4-RD) is a fibroinflammatory disorder which has been first reported in 2001 by Hamano and colleagues in a patient with autoimmune sclerosing pancreatitis. Almost every organ in the human body can be affected by IgG4-RD from infiltration with IgG4-positive plasma cells. Involvement of lungs with IgG4 is reported previously, but still, there is no clear picture of the pathophysiology behind lung involvement. Here, we are presenting a patient who has IgG4-RD presenting as pseudotumor of the lungs.
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Agraval, Hina, and Hong Wei Chu. "Lung Organoids in Smoking Research: Current Advances and Future Promises." Biomolecules 12, no. 10 (October 12, 2022): 1463. http://dx.doi.org/10.3390/biom12101463.
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Tobacco smoking has been established to contribute to the pathogenesis of various respiratory diseases including chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. However, major hurdles in mechanistic studies on the role of smoking in human lungs remain in part due to the lack of ex vivo experimental models and ambiguous data from animal models that can best recapitulate the architecture and pathophysiology of the human lung. Recent development of the lung organoid culture system has opened new avenues for respiratory disease research as organoids are proving to be a sophisticated ex vivo model that functionally and structurally mimics the human lungs better than other traditionally used models. This review will discuss how recent advances in lung organoid systems may help us better determine the injurious and immunological effect of smoking on human lungs and will provide some suggestions for future research directions.
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Das, Mita, W. Michael Zawada, James West, and Kurt R. Stenmark. "JNK2 regulates vascular remodeling in pulmonary hypertension." Pulmonary Circulation 8, no. 3 (May 2, 2018): 204589401877815. http://dx.doi.org/10.1177/2045894018778156.
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Pulmonary arterial (PA) wall modifications are key pathological features of pulmonary hypertension (PH). Although such abnormalities correlate with heightened phosphorylation of c-Jun N-terminal kinases 1/2 (JNK1/2) in a rat model of PH, the contribution of specific JNK isoforms to the pathophysiology of PH is unknown. Hence, we hypothesized that activation of either one, or both JNK isoforms regulates PA remodeling in PH. We detected increased JNK1/2 phosphorylation in the thickened vessels of PH patients’ lungs compared to that in lungs of healthy individuals. JNK1/2 phosphorylation paralleled a marked reduction in MAP kinase phosphatase 1 (JNK dephosphorylator) expression in patients’ lungs. Association of JNK1/2 activation with vascular modification was confirmed in the calf model of severe hypoxia-induced PH. To ascertain the role of each JNK isoform in pathophysiology of PH, wild-type (WT), JNK1 null (JNK1-/-), and JNK2 null (JNK2-/-) mice were exposed to chronic hypoxia (10% O2 for six weeks) to develop PH. In hypoxic WT lungs, an increase in JNK1/2 phosphorylation was associated with PH-like pathology. Hallmarks of PH pathophysiology, i.e. excessive accumulation of extracellular matrix and vessel muscularization with medial wall thickening, was also detected in hypoxic JNK1-/- lungs, but not in hypoxia-exposed JNK2-/- lungs. However, hypoxia-induced increases in right ventricular systolic pressure (RVSP) and in right ventricular hypertrophy (RVH) were similar in all three genotypes. Our findings suggest that JNK2 participates in PA remodeling (but likely not in vasoconstriction) in murine hypoxic PH and that modulating JNK2 actions might quell vascular abnormalities and limit the course of PH.
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Frétaud, Maxence, Delphyne Descamps, Daphné Laubreton, Marie-Anne Rameix-Welti, Jean-François Eléouët, Thibaut Larcher, Marie Galloux, and Christelle Langevin. "New Look at RSV Infection: Tissue Clearing and 3D Imaging of the Entire Mouse Lung at Cellular Resolution." Viruses 13, no. 2 (January 28, 2021): 201. http://dx.doi.org/10.3390/v13020201.
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Background: Respiratory Syncytial Virus (RSV) is the major cause of severe acute respiratory tract illness in young children worldwide and a main pathogen for the elderly and immune-compromised people. In the absence of vaccines or effective treatments, a better characterization of the pathogenesis of RSV infection is required. To date, the pathophysiology of the disease and its diagnosis has mostly relied on chest X-ray and genome detection in nasopharyngeal swabs. The development of new imaging approaches is instrumental to further the description of RSV spread, virus–host interactions and related acute respiratory disease, at the level of the entire lung. Methods: By combining tissue clearing, 3D microscopy and image processing, we developed a novel visualization tool of RSV infection in undissected mouse lungs. Results: Whole tissue analysis allowed the identification of infected cell subtypes, based on both morphological traits and position within the cellular network. Furthermore, 3D imaging was also valuable to detect the cytoplasmic viral factories, also called inclusion bodies, a hallmark of RSV infection. Conclusions: Whole lung clearing and 3D deep imaging represents an unprecedented visualization method of infected lungs to allow insight into RSV pathophysiology and improve the 2D histology analyses.
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Raredon, Micha Sam Brickman, Taylor Sterling Adams, Yasir Suhail, Jonas Christian Schupp, Sergio Poli, Nir Neumark, Katherine L. Leiby, et al. "Single-cell connectomic analysis of adult mammalian lungs." Science Advances 5, no. 12 (December 2019): eaaw3851. http://dx.doi.org/10.1126/sciadv.aaw3851.
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Efforts to decipher chronic lung disease and to reconstitute functional lung tissue through regenerative medicine have been hampered by an incomplete understanding of cell-cell interactions governing tissue homeostasis. Because the structure of mammalian lungs is highly conserved at the histologic level, we hypothesized that there are evolutionarily conserved homeostatic mechanisms that keep the fine architecture of the lung in balance. We have leveraged single-cell RNA sequencing techniques to identify conserved patterns of cell-cell cross-talk in adult mammalian lungs, analyzing mouse, rat, pig, and human pulmonary tissues. Specific stereotyped functional roles for each cell type in the distal lung are observed, with alveolar type I cells having a major role in the regulation of tissue homeostasis. This paper provides a systems-level portrait of signaling between alveolar cell populations. These methods may be applicable to other organs, providing a roadmap for identifying key pathways governing pathophysiology and informing regenerative efforts.
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Meyerowitz, Glen, and Igor Barjaktarevic. "369 The impact of asymmetric lung injury on gas and pressures distribution in a mechanical ventilation model with implementation of compartmentalized inspiratory hold." Journal of Clinical and Translational Science 6, s1 (April 2022): 69. http://dx.doi.org/10.1017/cts.2022.209.
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OBJECTIVES/GOALS: Asymmetries in lung pathophysiology can result in a maldistribution of gas between regions of the lungs which may generate dangerous pressures that are not observable by clinicians. Our study aims to demonstrate and quantify this through use of high-fidelity simulators to represent a range of commonly encountered clinical pathologies. METHODS/STUDY POPULATION: A benchtop study was performed with two high-fidelity breathing simulators, each representing one lung. This system allows for real-time monitoring of pressure and lung dynamics in a two-lung asymmetric injury model. One simulator was set to a fixed compliance and a resistance. A second simulator had a range of compliance and resistance values. Data were collected for 15 different test cases across a distribution of asymmetries. Each test case is run for 30 cycles. At the end of each ventilatory cycle, a short expiratory hold is performed, allowing pressure in the lung simulator, tubing, and ventilator circuit to equilibrate between cycles. RESULTS/ANTICIPATED RESULTS: Maldistribution of tidal volume was demonstrated when the compliance ratio between lung models (CL1/CL2) was 0.2 and the resistance ratio (RL1/RL2) was 10 with 23.9% (99% CI: 23.9-24.0%) of the gas volume distributed to lung 1 (103 mL L1 vs 327 mL in L2). Additionally, the injured lung when compared with the normal lung experienced higher peak pressures (12.8 cm H2O vs. 6.9 cm H2O, L1 and L2 respectively) and higher compartmentalized plateau pressures (11.5 cm H2O vs. 6.8 cm H2O, L1 and L2 respectively). DISCUSSION/SIGNIFICANCE: We demonstrate significant maldistribution of volume and pressures between two lungs in an asymmetric injury model. This study suggests significant impact of asymmetry in current lung-protective mechanical ventilation strategies and calls for better understanding of case-specific pathophysiologic changes affecting each of the two lungs.
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Chacón-Aponte, Ariana Alejandra, Érika Andrea Durán-Vargas, Jaime Adolfo Arévalo-Carrillo, Iván David Lozada-Martínez, Maria Paz Bolaño-Romero, Luis Rafael Moscote-Salazar, Pedro Grille, and Tariq Janjua. "Brain-lung interaction: a vicious cycle in traumatic brain injury." Acute and Critical Care 37, no. 1 (February 28, 2022): 35–44. http://dx.doi.org/10.4266/acc.2021.01193.
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The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.
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Greenspan, Jay, Thomas Miller, and Thomas Shaffer. "The Neonatal Respiratory Pump: A Developmental Challenge with Physiologic Limitations." Neonatal Network 24, no. 5 (September 2005): 15–22. http://dx.doi.org/10.1891/0730-0832.24.5.15.
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Newborn lungs are particularly susceptible to pathophysiology. Respiratory distress commonly brings infants to the intensive care nursery. Premature birth compromises the infant’s ability to respond to early lung dysfunction because of the reduced functional reserve available at younger gestational ages. The respiratory pump consists of respiratory musculature and the chest wall. The respiratory pump is the physiologic “machine” that responds to lung pathology. From gestation onward, components of the pump undergo developmental changes that influence its compensatory ability in the neonate. Careful observation of the synchrony of the chest wall and abdomen during spontaneous breathing efforts assists the caretaker in detecting respiratory compromise and impending respiratory failure. Noninvasive monitoring of respiratory patterns is a valuable tool for the neonatal caregiver, who must understand the developmental changes in the respiratory pump and be able to identify an infant’s ineffective responses to lung pathophysiology.
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Armstead, Valerie E., Irina L. Opentanova, Alexander G. Minchenko, and Allan M. Lefer. "Tissue Factor Expression in Vital Organs during Murine Traumatic Shock." Anesthesiology 91, no. 6 (December 1, 1999): 1844. http://dx.doi.org/10.1097/00000542-199912000-00039.
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Background Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats. Methods Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger RNA (mRNA) was measured in the lung, liver, and small intestine using ribonuclease protection assays. Electromobility shift assays were used to quantify binding of nuclear extracts from lung to TF-specific consensus domains for transcription factors NF-kappaB and AP-1. Results TF activity in plasma increased up to 14-fold and +232% in the lung (P < 0.001 for plasma and lung) 2 h after trauma. TF mRNA level was significantly increased in the lungs (P < 0.01), small intestine (P < 0.01), and liver (P < 0.05) 1 h after trauma compared to sham-operated control rats. TF mRNA expression continued to increase in the lungs and the liver (both, P < 0.001) 2 h after trauma TF sequence-specific complex binding to AP-1 and NF-kappaB domains was enhanced in the lungs of trauma rats (+395%, P < 0.001 and +168%, P < 0.001, respectively). Conclusions These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock.
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Romero-Lopez, Maria del Mar, Marc Oria, Miki Watanabe-Chailland, Maria Florencia Varela, Lindsey Romick-Rosendale, and Jose L. Peiro. "Lung Metabolomics Profiling of Congenital Diaphragmatic Hernia in Fetal Rats." Metabolites 11, no. 3 (March 18, 2021): 177. http://dx.doi.org/10.3390/metabo11030177.
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Congenital diaphragmatic hernia (CDH) is characterized by the herniation of abdominal contents into the thoracic cavity during the fetal period. This competition for fetal thoracic space results in lung hypoplasia and vascular maldevelopment that can generate severe pulmonary hypertension (PH). The detailed mechanisms of CDH pathogenesis are yet to be understood. Acknowledgment of the lung metabolism during the in-utero CDH development can help to discern the CDH pathophysiology changes. Timed-pregnant dams received nitrofen or vehicle (olive oil) on E9.5 day of gestation. All fetal lungs exposed to nitrofen or vehicle control were harvested at day E21.5 by C-section and processed for metabolomics analysis using nuclear magnetic resonance (NMR) spectroscopy. The three groups analyzed were nitrofen-CDH (NCDH), nitrofen-control (NC), and vehicle control (VC). A total of 64 metabolites were quantified and subjected to statistical analysis. The multivariate analysis identified forty-four metabolites that were statistically different between the three groups. The highest Variable importance in projection (VIP) score (>2) metabolites were lactate, glutamate, and adenosine 5′-triphosphate (ATP). Fetal CDH lungs have changes related to oxidative stress, nucleotide synthesis, amino acid metabolism, glycerophospholipid metabolism, and glucose metabolism. This work provides new insights into the molecular mechanisms behind the CDH pathophysiology and can explore potential novel treatment targets for CDH patients.
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Reddy, R. Chandramouli, Basavaraj Devaranavadagi, and Kusal K. Das. "Nickel Induced Alteration of Pathophysiology of Lungs in Experimental Rats." Indian Journal of Public Health Research & Development 10, no. 8 (2019): 145. http://dx.doi.org/10.5958/0976-5506.2019.01867.9.
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Peterson, Steven. "Understanding the Sequence of Pulmonary Injury in the Extremely Low Birth Weight, Surfactant-Deficient Infant." Neonatal Network 28, no. 4 (July 2009): 221–29. http://dx.doi.org/10.1891/0730-0832.28.4.221.
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Human lung development begins around day 26 postconception and continues throughout early childhood. Many crucial events can affect this delicate tissue as it develops, leading to altered and abnormal growth and development of the lungs, thereby yielding a variety of morbidities and sometimes even mortality. Understanding the pathophysiology of lung injury in the extremely low birth weight neonate is essential when caring for these infants, especially during the first hours of life. This article provides bedside clinicians with foundational information related to acute lung injury and the sequence of events that can ultimately lead to neonatal chronic lung disease and bronchopulmonary dysplasia.
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Amariei, Diana E., Neal Dodia, Janaki Deepak, Stella E. Hines, Jeffrey R. Galvin, Sergei P. Atamas, and Nevins W. Todd. "Combined Pulmonary Fibrosis and Emphysema: Pulmonary Function Testing and a Pathophysiology Perspective." Medicina 55, no. 9 (September 10, 2019): 580. http://dx.doi.org/10.3390/medicina55090580.
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Combined pulmonary fibrosis and emphysema (CPFE) has been increasingly recognized over the past 10–15 years as a clinical entity characterized by rather severe imaging and gas exchange abnormalities, but often only mild impairment in spirometric and lung volume indices. In this review, we explore the gas exchange and mechanical pathophysiologic abnormalities of pulmonary emphysema, pulmonary fibrosis, and combined emphysema and fibrosis with the goal of understanding how individual pathophysiologic observations in emphysema and fibrosis alone may impact clinical observations on pulmonary function testing (PFT) patterns in patients with CPFE. Lung elastance and lung compliance in patients with CPFE are likely intermediate between those of patients with emphysema and fibrosis alone, suggesting a counter-balancing effect of each individual process. The outcome of combined emphysema and fibrosis results in higher lung volumes overall on PFTs compared to patients with pulmonary fibrosis alone, and the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio in CPFE patients is generally preserved despite the presence of emphysema on chest computed tomography (CT) imaging. Conversely, there appears to be an additive deleterious effect on gas exchange properties of the lungs, reflecting a loss of normally functioning alveolar capillary units and effective surface area available for gas exchange, and manifested by a uniformly observed severe reduction in the diffusing capacity for carbon monoxide (DLCO). Despite normal or only mildly impaired spirometric and lung volume indices, patients with CPFE are often severely functionally impaired with an overall rather poor prognosis. As chest CT imaging continues to be a frequent imaging modality in patients with cardiopulmonary disease, we expect that patients with a combination of pulmonary emphysema and pulmonary fibrosis will continue to be observed. Understanding the pathophysiology of this combined process and the abnormalities that manifest on PFT testing will likely be helpful to clinicians involved with the care of patients with CPFE.
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Kosutova, P., and P. Mikolka. "Aspiration syndromes and associated lung injury: incidence, pathophysiology and management." Physiological Research, S4 (December 30, 2021): S567—S583. http://dx.doi.org/10.33549//physiolres.934767.
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Aspiration is a common condition affecting healthy or sick patients which could create an acute or chronic inflammatory reaction in the lungs. Aspiration syndromes could be categorized according to a content entering the respiratory system into bacterial aspiration pneumonia with the gastric or oropharyngeal bacteria entering, aspiration chemical pneumonitis with bacteria-freegastric acid aspiration, or aspiration of a foreign body which causes an acute pulmonary emergency. There are differences in the clinical presentation of volume-dependent aspirations (microaspiration and macroaspiration): the higher is the volume of aspiration, the greater is the injury to the patient and more serious are the health consequences (with 70 % mortality rate for hospitalized patients). Aspiration syndromes can affect both the airways and pulmonary parenchyma, leading to acute lung injury, increased hospitalization rate and worse outcomes in critically ill patients. Impaired alveolar-capillary permeability, oedema formation, neutrophilic inflammatory response and pulmonary surfactant inactivation lead to reduced lung compliance and loss of aerated lung tissue and give rise to hypoxemia and respiratory failure. This review discusses the effect of aspiration events on the pulmonary tissue. The main focus is to distinguish the differences between bacterial and chemical pneumonia, their clinical presentation and symptoms, risk factors of developing the changes, possibilities of diagnostics and management as well as prevention of aspirations. Because of a risk of serious lung damage after the aspiration, pathophysiology and processes leading to lung tissue injury are discussed in detail. Data sources represent a systematic literature search using relevant medical subject headings.
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Marčetić, Dejan, Miroslav Samaržija, Andrea Vukić Dugac, and Jelena Knežević. "Angiotensin-Converting Enzyme 2 (ACE2) as a Potential Diagnostic and Prognostic Biomarker for Chronic Inflammatory Lung Diseases." Genes 12, no. 7 (July 9, 2021): 1054. http://dx.doi.org/10.3390/genes12071054.
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Chronic inflammatory lung diseases are characterized by uncontrolled immune response in the airways as their main pathophysiological manifestation. The lack of specific diagnostic and therapeutic biomarkers for many pulmonary diseases represents a major challenge for pulmonologists. The majority of the currently approved therapeutic approaches are focused on achieving disease remission, although there is no guarantee of complete recovery. It is known that angiotensin-converting enzyme 2 (ACE2), an important counter-regulatory component of the renin–angiotensin–aldosterone system (RAAS), is expressed in the airways. It has been shown that ACE2 plays a role in systemic regulation of the cardiovascular and renal systems, lungs and liver by acting on blood pressure, electrolyte balance control mechanisms and inflammation. Its protective role in the lungs has also been presented, but the exact pathophysiological mechanism of action is still elusive. The aim of this study is to review and discuss recent findings about ACE2, including its potential role in the pathophysiology of chronic inflammatory lung diseases:, i.e., chronic obstructive pulmonary disease, asthma, and pulmonary hypertension. Additionally, in the light of the coronavirus 2019 disease (COVID-19), we will discuss the role of ACE2 in the pathophysiology of this disease, mainly represented by different grades of pulmonary problems. We believe that these insights will open up new perspectives for the future use of ACE2 as a potential biomarker for early diagnosis and monitoring of chronic inflammatory lung diseases.
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Arrigo, Mattia, Lars Christian Huber, Stephan Winnik, Fran Mikulicic, Federica Guidetti, Michelle Frank, Andreas J. Flammer, and Frank Ruschitzka. "Right Ventricular Failure: Pathophysiology, Diagnosis and Treatment." Cardiac Failure Review 5, no. 3 (November 4, 2019): 140–46. http://dx.doi.org/10.15420/cfr.2019.15.2.
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The prognostic significance of the right ventricle (RV) has recently been recognised in several conditions, primarily those involving the left ventricle, the lungs and their vascular bed, or the right-sided chambers. Recent advances in imaging techniques have created new opportunities to study RV anatomy, physiology and pathophysiology, and contemporary research efforts have opened the doors to new treatment possibilities. Nevertheless, the treatment of RV failure remains challenging. Optimal management should consider the anatomical and physiological particularities of the RV and include appropriate imaging techniques to understand the underlying pathophysiological mechanisms. Treatment should include rapid optimisation of volume status, restoration of perfusion pressure and improvement of myocardial contractility and rhythm, and, in case of refractory RV failure, mechanical circulatory support.
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Barron, Luke, Amber Smith, Karim El Kasmi, Joseph Qualls, Xiaozhu Huang, Thomas Wynn, and Peter Murray. "Genetic analysis of arginase 1 in Th2-dominated lung inflammation (163.12)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 163.12. http://dx.doi.org/10.4049/jimmunol.186.supp.163.12.
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Abstract Arginase 1 (Arg1) expression in myeloid lineage cells, and especially alternatively-activated macrophages, increases dramatically in the lungs of mice with acute and chronic Th2-driven inflammation. Arg1 has been proposed to contribute to asthma pathogenesis by regulating at least four pathways: inhibiting the production of nitric oxide by substrate competition, regulating fibrosis and polyamine supply, regulating the bioavailability of arginine in the lung, and inhibiting T cell proliferation. Here we used mice lacking Arg1 in myeloid lineage cells, to investigate the contribution of Arg1 to asthma pathophysiology and lung inflammation. In six distinct model systems encompassing acute and chronic Th2-mediated inflammation, we observed neither a pathogenic nor protective role for myeloid-expressed Arg1 in any measured parameter of lung pathophysiology. Collectively, our results argue that (i) attempts to inhibit arginases in the lung by small molecule arginase inhibitors or RNAi should be examined with caution and (ii) whether macrophages use Arg1 to limit Th2 responses depends on the organ and type of infection or injury.
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Kelsey, Ryan, Fiona N. Manderson Koivula, Neville H. McClenaghan, and Catriona Kelly. "Cystic Fibrosis–Related Diabetes: Pathophysiology and Therapeutic Challenges." Clinical Medicine Insights: Endocrinology and Diabetes 12 (January 2019): 117955141985177. http://dx.doi.org/10.1177/1179551419851770.
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Cystic fibrosis–related diabetes (CFRD) is among the most common extrapulmonary co-morbidity associated with cystic fibrosis (CF), affecting an estimated 50% of adults with the condition. Cystic fibrosis is prevalent in 1 in every 2500 Caucasian live births and is caused by a mutation in the cystic fibrosis transmembrane conductance regulator ( CFTR) gene. Mutated CFTR leads to dehydrated epithelial surfaces and a build-up of mucus in a variety of tissues including the lungs and pancreas. The leading cause of mortality in CF is repeated respiratory bacterial infections, which prompts a decline in lung function. Co-morbid diabetes promotes bacterial colonisation of the airways and exacerbates the deterioration in respiratory health. Cystic fibrosis–related diabetes is associated with a 6-fold higher mortality rate compared with those with CF alone. The management of CFRD adds a further burden for the patient and creates new therapeutic challenges for the clinical team. Several proposed hypotheses on how CFRD develops have emerged, including exocrine-driven fibrosis and destruction of the entire pancreas and contrasting theories on the direct or indirect impact of CFTR mutation on islet function. The current review outlines recent data on the impact of CFTR on endocrine pancreatic function and discusses the use of conventional diabetic therapies and new CFTR-correcting drugs on the treatment of CFRD.
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Misra, Vikas, Hannah Lee, Anju Singh, Kewu Huang, Rajesh K. Thimmulappa, Wayne Mitzner, Shyam Biswal, and Clarke G. Tankersley. "Global expression profiles from C57BL/6J and DBA/2J mouse lungs to determine aging-related genes." Physiological Genomics 31, no. 3 (November 2007): 429–40. http://dx.doi.org/10.1152/physiolgenomics.00060.2007.
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This study identified gene expression profiles that provided evidence for genomic mechanisms underlying the pathophysiology of aging lung. Aging lungs from C57BL/6 (B6) and DBA/2 (D2) mouse strains differ in physiology and morphometry. Lungs were harvested from B6 mice at 2, 18, and 26 mo and from D2 mice at 2 and 18 mo of age. Purified RNA was subjected to oligonucleotide microarray analyses, and differential expression analyses were performed for comparison of various data sets. A significant majority of differentially expressed genes were upregulated with aging in both strains. Aging D2 lungs uniquely exhibited upregulation in stress-response genes including xenobiotic detoxification cascades. In contrast, aging B6 lungs showed downregulation of heat shock-response genes. Age-dependent downregulation of genes common to both B6 and D2 strains included several collagen genes (e.g., Col1a1 and Col3a1). There was a greater elastin gene ( Eln) expression in D2 mice at 2 mo, and Eln was uniquely downregulated with age in this strain. The matrix metalloproteinase 14 gene ( Mmp14), critical to alveolar structural integrity, was also downregulated with aging in D2 mice only. Several polymorphisms in the regulatory and untranslated regions of Mmp14 were identified between strains, suggesting that variation in Mmp14 gene regulation contributes to accelerated aging of lungs in D2 mice. In summary, lungs of B6 and D2 mice age with variable rates at the gene expression level, and these quantifiable genomic differences provide a template for understanding the variability in age-dependent changes in lung structure and function.
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Lindsey, Ashley S., Lydia M. Sullivan, Nicole A. Housley, Anna Koloteva, Judy A. King, Jonathon P. Audia, and Diego F. Alvarez. "Analysis of pulmonary vascular injury and repair during Pseudomonas aeruginosa infection-induced pneumonia and acute respiratory distress syndrome." Pulmonary Circulation 9, no. 1 (January 2019): 204589401982694. http://dx.doi.org/10.1177/2045894019826941.
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Herein we describe lung vascular injury and repair using a rodent model of Pseudomonas aeruginosa pneumonia-induced acute respiratory distress syndrome (ARDS) during: 1) the exudative phase (48-hour survivors) and 2) the reparative/fibro-proliferative phase (1-week survivors). Pneumonia was induced by intratracheal instillation of P. aeruginosa strain PA103, and lung morphology and pulmonary vascular function were determined subsequently. Pulmonary vascular function was assessed in mechanically ventilated animals in vivo (air dead space, PaO2, and lung mechanics) and lung permeability was determined in isolated perfused lungs ex vivo (vascular filtration coefficient and extravascular lung water). At 48 hours post infection, histological analyses demonstrated capillary endothelial disruption, diffuse alveolar damage, perivascular cuffs, and neutrophil influx into lung parenchyma. Infected animals displayed clinical hallmarks of ARDS, including increased vascular permeability, increased dead space, impaired gas exchange, and decreased lung compliance. Overall, the animal infection model recapitulated the morphological and functional changes typically observed in lungs from patients during the exudative phase of ARDS. At 1 week post infection, there was lung histological and pulmonary vascular functional evidence of repair when compared with 48 hours post infection; however, some parameters were still impaired when compared with uninfected controls. Importantly, lungs displayed increased fibrosis and cellular hyperplasia reminiscent of lungs from patients during the fibro-proliferative phase of ARDS. Control, sham inoculated animals showed normal lung histology and function. These data represent the first comprehensive assessment of lung pathophysiology during the exudative and reparative/fibro-proliferative phases of P. aeruginosa pneumonia-induced ARDS, and position this pre-clinical model for use in interventional studies aimed at advancing clinical care.
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Wagers, Scott, Lennart K. A. Lundblad, Mari Ekman, Charles G. Irvin, and Jason H. T. Bates. "The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?" Journal of Applied Physiology 96, no. 6 (June 2004): 2019–27. http://dx.doi.org/10.1152/japplphysiol.00924.2003.
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Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we show that the hyperresponsiveness of mice with allergically inflamed airways can be explained entirely by a thickening of the airway mucosa and an increased propensity of the airways to close, without the involvement of any increase in the degree of airway smooth muscle shortening. This has implications for the pathophysiology of asthma and suggests that at least some types of asthma may benefit from therapies aimed at manipulating surface tension at the air-liquid interface in the lungs.
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Galaris, Apostolos, Dionysios Fanidis, Elli-Anna Stylianaki, Vaggelis Harokopos, Alexandra-Styliani Kalantzi, Panagiotis Moulos, Antigone S. Dimas, Pantelis Hatzis, and Vassilis Aidinis. "Obesity Reshapes the Microbial Population Structure along the Gut-Liver-Lung Axis in Mice." Biomedicines 10, no. 2 (February 19, 2022): 494. http://dx.doi.org/10.3390/biomedicines10020494.
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The microbiome is emerging as a major player in tissue homeostasis in health and disease. Gut microbiome dysbiosis correlates with several autoimmune and metabolic diseases, while high-fat diets and ensuing obesity are known to affect the complexity and diversity of the microbiome, thus modulating pathophysiology. Moreover, the existence of a gut-liver microbial axis has been proposed, which may extend to the lung. In this context, we systematically compared the microbiomes of the gut, liver, and lung of mice fed a high-fat diet to those of littermates fed a matched control diet. We carried out deep sequencing of seven hypervariable regions of the 16S rRNA microbial gene to examine microbial diversity in the tissues of interest. Comparison of the local microbiomes indicated that lung tissue has the least diverse microbiome under healthy conditions, while microbial diversity in the healthy liver clustered closer to the gut. Obesity increased microbial complexity in all three tissues, with lung microbial diversity being the most modified. Obesity promoted the expansion of Firmicutes along the gut-liver-lung axis, highlighting staphylococcus as a possible pathologic link between obesity and systemic pathophysiology, especially in the lungs.
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Lindholm, Peter, and Claes EG Lundgren. "The physiology and pathophysiology of human breath-hold diving." Journal of Applied Physiology 106, no. 1 (January 2009): 284–92. http://dx.doi.org/10.1152/japplphysiol.90991.2008.
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This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hemorrhage postdive. However, a remarkable, and so far poorly understood, variation in individual disposition for such problems exists. Mortality connected with breath-hold diving is primarily concentrated to less well-trained recreational divers and competitive spearfishermen who fall victim to hypoxia. Particularly vulnerable are probably also individuals with preexisting cardiac problems and possibly, essentially healthy divers who may have suffered severe alternobaric vertigo as a complication to inadequate pressure equilibration of the middle ears. The specific topics discussed include the diving response and its expression by the cardiovascular system, which exhibits hypertension, bradycardia, oxygen conservation, arrhythmias, and contraction of the spleen. The respiratory system is challenged by compression of the lungs with barotrauma of descent, intrapulmonary hemorrhage, edema, and the effects of glossopharyngeal insufflation and exsufflation. Various mechanisms associated with hypoxia and loss of consciousness are discussed, including hyperventilation, ascent blackout, fasting, and excessive postexercise O2 consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N2 narcosis is also illuminated.
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Hirleman, E., and DF Larson. "Cardiopulmonary bypass and edema: physiology and pathophysiology." Perfusion 23, no. 6 (November 2008): 311–22. http://dx.doi.org/10.1177/0267659109105079.
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Edema is a common morbidity following cardiopulmonary bypass (CPB) and can result in injury to many organs, including the heart, lungs, and brain. Generalized edema is also common and can lead to increased post-operative hospital stay and other morbidities. Pediatric patients are more susceptible to post-CPB edema and the consequences are more severe for this population. Hemodilution and systemic inflammatory responses are two suspected causes of CPB-related edema; however, the mechanisms involved are far from understood. Also, the common strategies to improve edema have not been completely successful and there is a need for new strategies at maintaining a fluid balance of patients as close to physiological as possible, especially for pediatric patients. An integrative approach to understanding edema is necessary as the forces involved in fluid homeostasis are dynamic and interdependent. Therefore, this review will focus on the physiology of fluid homeostasis and the pathologies of fluid shifts during CPB which lead to general edema as well as tissue-specific edema.
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Wright, Joseph K., Lawrence T. Kim, Thomas E. Rogers, and Richard H. Turnage. "Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1167–74. http://dx.doi.org/10.1152/jappl.2000.88.4.1167.
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The induction of cyclooxygenase is an important event in the pathophysiology of acute lung injury. The purpose of this study was to examine the synergistic effects of various cyclooxygenase products (PGE2, PGI2, PGF2α) on thromboxane A2(TxA2)-mediated pulmonary microvascular dysfunction. The lungs of Sprague-Dawley rats were perfused ex vivo with Krebs-Henseleit buffer containing indomethacin and PGE2 (5 × 10− 8 to 1 × 10− 7 M), PGF2α (7 × 10− 9 to 5 × 10− 6 M), or PGI2 (5 × 10− 8 to 2 × 10− 5 M). The TxA2-receptor agonist U-46619 (7 × 10− 8 M) was then added to the perfusate, and then the capillary filtration coefficient ( K f), pulmonary arterial pressure (Ppa), and total pulmonary vascular resistance (Rt) were determined. The K f of lungs perfused with U-46619 was twice that of lungs perfused with buffer alone ( P = 0.05). The presence of PGE2, PGF2α, and PGI2 within the perfusate of lungs exposed to U-46619 caused 118, 65, and 68% increases in K f, respectively, over that of lungs perfused with U-46619 alone ( P < 0.03). The Rt of lungs perfused with PGE2 + U-46619 was ∼30% greater than that of lungs exposed to either U-46619 ( P < 0.02) or PGE2 ( P < 0.01) alone. When paired measurements of Rt taken before and then 15 min after the addition of U-46619 were compared, PGI2 was found to attenuate U-46619-induced increases in Rt ( P < 0.01). These data suggest that PGE2, PGI2, and PGF2α potentiate the effects of TxA2-receptor activation on pulmonary microvascular permeability.
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Ambrosetti, Maria-Chiara, Giulia Battocchio, Stefania Montemezzi, Filippo Cattazzo, Tissjana Bejko, Evelina Tacconelli, Pietro Minuz, Ernesto Crisafulli, Cristiano Fava, and Giancarlo Mansueto. "The Caliber of Segmental and Subsegmental Vessels in COVID-19 Pneumonia Is Enlarged: A Distinctive Feature in Comparison with Other Forms of Inflammatory and Thromboembolic Diseases." Journal of Personalized Medicine 12, no. 9 (September 7, 2022): 1465. http://dx.doi.org/10.3390/jpm12091465.
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Background: The purpose of this study was to compare COVID-19 patients’ vessel caliber with that of normal lungs and lungs affected by other inflammatory and thromboembolic processes. Methods: between March and April 2020, 42 patients affected by COVID-19 pneumonia (COV-P) underwent CT scans of the lungs at Verona University Hospital for clinical indications. The lung images of four different groups of patients were compared (normal lung (NL), distal thromboembolism (DTE), and bacterial and fungal pneumonia (Bact-P, Fung-P)) by a radiologist with four years of experience. Results: The COV-P patients’ segmental and subsegmental vessels, evaluated as the ratio with the corresponding bronchial branch (V/B ratio), were larger, with respect to the NL the DTE groups, in the apparently healthy parenchyma, a result confirmed in the zones of opacification with respect to the Bact-P and Fung-P groups. Conclusions: This was the first study to show, by comparative analysis, that COVID-19 patients’ segmental and subsegmental vessel calibers are significantly enlarged. This is a distinctive feature of COVID-19 pneumonia, suggesting its distinct pathophysiology as compared to other inflammatory and thromboembolic diseases and alerting radiologists to consider it when evaluating the CT scans of suspected patients.
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Nielsen, O. S., A. J. Munro, and I. F. Tannock. "Bone metastases: pathophysiology and management policy." Journal of Clinical Oncology 9, no. 3 (March 1991): 509–24. http://dx.doi.org/10.1200/jco.1991.9.3.509.
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The pathophysiology and options for management of bone metastases as well as criteria for determining response to therapy are reviewed. Bone metastases are frequently one of the first signs of disseminated disease in cancer patients. In the majority of patients, the primary tumor is in the breast, prostate, or lungs. Although almost all patients will die of their disease, a proportion of the patients will survive for several years. Treatment is primarily palliative: the intention is to relieve pain, prevent fractures, maintain activity and mobility, and, if possible, to prolong survival. Therapeutic options include local treatment with radiotherapy and/or surgery, and systemic treatment using chemotherapy, endocrine therapy, radioisotopes, agents such as diphosphonates, which inhibit resorption of bone, as well as analgesic and antiinflammatory drugs. The mechanisms by which pain is relieved by several of these therapies remain unclear but actions beyond a simple tumoricidal effect appear to be important. There have been few randomized trials comparing the therapeutic options, and the criteria for assessing response to therapy have, in general, been poorly defined. There is a need for rigorous clinical investigations that assess the efficacy of the various therapeutic possibilities by using well-defined and validated criteria of response.
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Marney, Samuel R. "Pathophysiology of Reactive Airway Disease and Sinusitis." Annals of Otology, Rhinology & Laryngology 105, no. 2 (February 1996): 98–100. http://dx.doi.org/10.1177/000348949610500203.
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The association between asthma and sinusitis was recognized more than a century ago. Since 1980, several studies have documented that severe asthma improved after coexisting sinusitis was effectively treated either medically or surgically. Because the mechanism relating sinusitis to asthma is not known, several theories have been proposed: 1) aspiration of infected sinus secretions into the lungs during sleep, 2) enhanced vagal stimulation in the infected sinus producing direct bronchospasm, 3) bronchospasm from excessive airway drying from mouth breathing, 4) production of bacterial toxins that induce partial beta blockade, and 5) production in the infected sinus of cytokines and bronchoconstrictive mediators. There are data to support each of these hypotheses, and any or all of them may be operative. In view of recent demonstrations of activated lymphocytes and eosinophils in asthmatic airways, it is intriguing that biopsies of chronic hypertrophic sinusitis have revealed increased numbers of eosinophils and increased levels of granulocyte-macrophage colony stimulating factor, interleukin-3, and interleukin-5 compared to control tissue. These findings suggest that sinusitis might induce asthma by stimulating eosinophil production and activation and thereby supplying peptidoleukotrienes (LTC4 and LTD4) and other asthmagenic eosinophil products.
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Poloni, Tino Emanuele, Matteo Moretti, Valentina Medici, Elvira Turturici, Giacomo Belli, Elena Cavriani, Silvia Damiana Visonà, et al. "COVID-19 Pathology in the Lung, Kidney, Hearts and Brain: The Different Roles of T-Cells, Macrophages, and Microthrombosis." Cells 11, no. 19 (October 4, 2022): 3124. http://dx.doi.org/10.3390/cells11193124.
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Here, we aim to describe COVID-19 pathology across different tissues to clarify the disease’s pathophysiology. Lungs, kidneys, hearts, and brains from nine COVID-19 autopsies were compared by using antibodies against SARS-CoV-2, macrophages-microglia, T-lymphocytes, B-lymphocytes, and activated platelets. Alzheimer’s Disease pathology was also assessed. PCR techniques were used to verify the presence of viral RNA. COVID-19 cases had a short clinical course (0–32 days) and their mean age was 77.4 y/o. Hypoxic changes and inflammatory infiltrates were present across all tissues. The lymphocytic component in the lungs and kidneys was predominant over that of other tissues (p < 0.001), with a significantly greater presence of T-lymphocytes in the lungs (p = 0.020), which showed the greatest presence of viral antigens. The heart showed scant SARS-CoV-2 traces in the endothelium–endocardium, foci of activated macrophages, and rare lymphocytes. The brain showed scarce SARS-CoV-2 traces, prominent microglial activation, and rare lymphocytes. The pons exhibited the highest microglial activation (p = 0.017). Microthrombosis was significantly higher in COVID-19 lungs (p = 0.023) compared with controls. The most characteristic pathological features of COVID-19 were an abundance of T-lymphocytes and microthrombosis in the lung and relevant microglial hyperactivation in the brainstem. This study suggests that the long-term sequelae of COVID-19 derive from persistent inflammation, rather than persistent viral replication.
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Roque, Willy, Alexandra Boni, Jose Martinez-Manzano, and Freddy Romero. "A Tale of Two Proteolytic Machines: Matrix Metalloproteinases and the Ubiquitin–Proteasome System in Pulmonary Fibrosis." International Journal of Molecular Sciences 21, no. 11 (May 29, 2020): 3878. http://dx.doi.org/10.3390/ijms21113878.
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Pulmonary fibrosis is a chronic and progressive lung disease characterized by the activation of fibroblasts and the irreversible deposition of connective tissue matrices that leads to altered pulmonary architecture and physiology. Multiple factors have been implicated in the pathogenesis of lung fibrosis, including genetic and environmental factors that cause abnormal activation of alveolar epithelial cells, leading to the development of complex profibrotic cascade activation and extracellular matrix (ECM) deposition. One class of proteinases that is thought to be important in the regulation of the ECM are the matrix metalloproteinases (MMPs). MMPs can be up- and down- regulated in idiopathic pulmonary fibrosis (IPF) lungs and their role depends upon their location and function. Furthermore, alterations in the ubiquitin-proteosome system (UPS), a major intracellular protein degradation complex, have been described in aging and IPF lungs. UPS alterations could potentially lead to the abnormal accumulation and deposition of ECM. A better understanding of the specific roles MMPs and UPS play in the pathophysiology of pulmonary fibrosis could potentially drive to the development of novel biomarkers that can be as diagnostic and therapeutic targets. In this review, we describe how MMPs and UPS alter ECM composition in IPF lungs and mouse models of pulmonary fibrosis, thereby influencing the alveolar epithelial and mesenchymal cell behavior. Finally, we discuss recent findings that associate MMPs and UPS interplay with the development of pulmonary fibrosis.
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Aghali, Arbi, Maunick Lefin Koloko Ngassie, Christina M. Pabelick, and Y. S. Prakash. "Cellular Senescence in Aging Lungs and Diseases." Cells 11, no. 11 (May 29, 2022): 1781. http://dx.doi.org/10.3390/cells11111781.
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Cellular senescence represents a state of irreversible cell cycle arrest occurring naturally or in response to exogenous stressors. Following the initial arrest, progressive phenotypic changes define conditions of cellular senescence. Understanding molecular mechanisms that drive senescence can help to recognize the importance of such pathways in lung health and disease. There is increasing interest in the role of cellular senescence in conditions such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) in the context of understanding pathophysiology and identification of novel therapies. Herein, we discuss the current knowledge of molecular mechanisms and mitochondrial dysfunction regulating different aspects of cellular senescence-related to chronic lung diseases to develop rational strategies for modulating the senescent cell phenotype in the lung for therapeutic benefit.
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Giucă, Adrian, Tea Gegenava, Carmen Marina Mihai, Ciprian Jurcuţ, Adrian Săftoiu, Diana Monica Gȋrniţă, Bogdan Alexandru Popescu, Nina Ajmone Marsan, and Ruxandra Jurcuț. "Sclerodermic Cardiomyopathy—A State-of-the-Art Review." Diagnostics 12, no. 3 (March 9, 2022): 669. http://dx.doi.org/10.3390/diagnostics12030669.
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Systemic sclerosis (SSc) is a chronic autoimmune disorder with unknown triggering factors, and complex pathophysiologic links which lead to fibrosis of skin and internal organs, including the heart, lungs, and gut. However, more than 100 years after the first description of cardiac disease in SSc, sclerodermic cardiomyopathy (SScCmp) is an underrecognized, occult disease with important adverse long-term prognosis. Laboratory tests, electrocardiography (ECG) and cardiovascular multimodality imaging techniques (transthoracic 2D and 3D echocardiography, cardiac magnetic resonance (CMR), and novel imaging techniques, including myocardial deformation analysis) provide new insights into the cardiac abnormalities in patients with SSc. This state-of-the-art review aims to stratify all the cardiac investigations needed to diagnose and follow-up the SScCmp, and discusses the epidemiology, risk factors and pathophysiology of this important cause of morbidity of the SSc patient.
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Sucre, Jennifer M. S., Dan Wilkinson, Preethi Vijayaraj, Manash Paul, Bruce Dunn, Jackelyn A. Alva-Ornelas, and Brigitte N. Gomperts. "A three-dimensional human model of the fibroblast activation that accompanies bronchopulmonary dysplasia identifies Notch-mediated pathophysiology." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 10 (May 15, 2016): L889—L898. http://dx.doi.org/10.1152/ajplung.00446.2015.
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Bronchopulmonary dysplasia (BPD) is a leading complication of premature birth and occurs primarily in infants delivered during the saccular stage of lung development. Histopathology shows decreased alveolarization and a pattern of fibroblast proliferation and differentiation to the myofibroblast phenotype. Little is known about the molecular pathways and cellular mechanisms that define BPD pathophysiology and progression. We have developed a novel three-dimensional human model of the fibroblast activation associated with BPD, and using this model we have identified the Notch pathway as a key driver of fibroblast activation and proliferation in response to changes in oxygen. Fetal lung fibroblasts were cultured on sodium alginate beads to generate lung organoids. After exposure to alternating hypoxia and hyperoxia, the organoids developed a phenotypic response characterized by increased α-smooth muscle actin (α-SMA) expression and other genes known to be upregulated in BPD and also demonstrated increased expression of downstream effectors of the Notch pathway. Inhibition of Notch with a γ-secretase inhibitor prevented the development of the pattern of cellular proliferation and α-SMA expression in our model. Analysis of human autopsy tissue from the lungs of infants who expired with BPD demonstrated evidence of Notch activation within fibrotic areas of the alveolar septae, suggesting that Notch may be a key driver of BPD pathophysiology.
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Bera, Monali, Bao Lu, Thomas Martin, Shun Cui, Craig Gerard, and Norma Gerard. "The C3a anaphylatoxin receptor is critical in the pathophysiology of RSV infection (49.2)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 49.2. http://dx.doi.org/10.4049/jimmunol.186.supp.49.2.
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Abstract Respiratory syncytial virus (RSV) is linked to severe lung disease and may lead to wheezing in infants. RSV infection in mice demonstrates infiltration of inflammatory cells, mucus cell metaplasia, and airway hyperresonsiveness (AHR) to methacholine. Previous studies demonstrated activation of complement by RSV. Other studies showed a requirement for C3 or C3a in AHR associated with antigen sensitization as well as inhalation of particulate matter. We hypothesized, therefore, that C3a is a critical component for the AHR associated with RSV infection. We found that mice lacking the C3aR (C3aR1-/-) do not develop AHR secondary to acute RSV infection in contrast to wild type mice. Further, viral clearance was accelerated in C3aR1-/-mice. The AHR phenotype was restored to wild type when C3aR1-/- mice were transplanted with wild type bone marrow cells,supporting a role for a hematopoetic cell type. T cells were the dominant cell type increased in the lungs of both wild type and C3aR1-/-mice following RSV infection, however, the increases in lung IL-23 and IL-17 were significantly lower in C3aR1-/-mice compared with wild type animals. Additionally the increased levels of the transcription factor RORγT, responsible for regulating IL17 synthesis, seen in wild type mice were greatly reduced in C3aR1-/- mice. Our findings identify a key role for activation of complement anaphylatoxin C3aR in the pathophysiology of RSV disease, and may help identify a therapeutic target in humans.
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Weinberg, Frank, Robert P. Dickson, Deepak Nagrath, and Nithya Ramnath. "The Lung Microbiome: A Central Mediator of Host Inflammation and Metabolism in Lung Cancer Patients?" Cancers 13, no. 1 (December 22, 2020): 13. http://dx.doi.org/10.3390/cancers13010013.
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Lung cancer is the leading cause of cancer-related death. Over the past 5–10 years lung cancer outcomes have significantly improved in part due to better treatment options including immunotherapy and molecularly targeted agents. Unfortunately, the majority of lung cancer patients do not enjoy durable responses to these new treatments. Seminal research demonstrated the importance of the gut microbiome in dictating responses to immunotherapy in melanoma patients. However, little is known regarding how other sites of microbiota in the human body affect tumorigenesis and treatment responses. The lungs were traditionally thought to be a sterile environment; however, recent research demonstrated that the lung contains its own dynamic microbiota that can influence disease and pathophysiology. Few studies have explored the role of the lung microbiome in lung cancer biology. In this review article, we discuss the links between the lung microbiota and cancer, with particular focus on immune responses, metabolism and strategies to target the lung microbiome for cancer prevention.
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Hadjicharalambous, Marina R., and Mark A. Lindsay. "Idiopathic Pulmonary Fibrosis: Pathogenesis and the Emerging Role of Long Non-Coding RNAs." International Journal of Molecular Sciences 21, no. 2 (January 14, 2020): 524. http://dx.doi.org/10.3390/ijms21020524.
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Idiopathic pulmonary fibrosis (IPF) is a progressive chronic disease characterized by excessing scarring of the lungs leading to irreversible decline in lung function. The aetiology and pathogenesis of the disease are still unclear, although lung fibroblast and epithelial cell activation, as well as the secretion of fibrotic and inflammatory mediators, have been strongly associated with the development and progression of IPF. Significantly, long non-coding RNAs (lncRNAs) are emerging as modulators of multiple biological processes, although their function and mechanism of action in IPF is poorly understood. LncRNAs have been shown to be important regulators of several diseases and their aberrant expression has been linked to the pathophysiology of fibrosis including IPF. This review will provide an overview of this emerging role of lncRNAs in the development of IPF.
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Kim, Suhee, Hee Jin Park, and Sang-Il Lee. "The Microbiome in Systemic Sclerosis: Pathophysiology and Therapeutic Potential." International Journal of Molecular Sciences 23, no. 24 (December 18, 2022): 16154. http://dx.doi.org/10.3390/ijms232416154.
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Systemic sclerosis (SSc), also known as scleroderma, is an autoimmune disease with unknown etiology characterized by multi-organ fibrosis. Despite substantial investigation on SSc-related cellular and molecular mechanisms, effective therapies are still lacking. The skin, lungs, and gut are the most affected organs in SSc, which act as physical barriers and constantly communicate with colonized microbiota. Recent reports have documented a unique microbiome signature, which may be the pathogenic trigger or driver of SSc. Since gut microbiota influences the efficacy and toxicity of oral drugs, evaluating drug–microbiota interactions has become an area of interest in disease treatment. The existing evidence highlights the potential of the microbial challenge as a novel therapeutic option in SSc. In this review, we have summarized the current knowledge about molecular mechanisms of SSc and highlighted the underlying role of the microbiome in SSc pathogenesis. We have also discussed the latest therapeutic interventions using microbiomes in SSc, including drug–microbiota interactions and animal disease models. This review aims to elucidate the pathophysiological connection and therapeutic potential of the microbiome in SSc. Insights into the microbiome will significantly improve our understanding of etiopathogenesis and developing therapeutics for SSc.
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Hirata, Kazuto, Hiroshi Kanazawa, and Hiroshi Kamoi. "IV. Clinical aspects of delayed hypersensitivity in lungs: Pathophysiology of hypersensitivity disorders in clinics." Microscopy Research and Technique 53, no. 4 (2001): 307–12. http://dx.doi.org/10.1002/jemt.1097.
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Forgie, Keir A., Nicholas Fialka, Darren H. Freed, and Jayan Nagendran. "Lung Transplantation, Pulmonary Endothelial Inflammation, and Ex-Situ Lung Perfusion: A Review." Cells 10, no. 6 (June 7, 2021): 1417. http://dx.doi.org/10.3390/cells10061417.
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Lung transplantation (LTx) is the gold standard treatment for end-stage lung disease; however, waitlist mortality remains high due to a shortage of suitable donor lungs. Organ quality can be compromised by lung ischemic reperfusion injury (LIRI). LIRI causes pulmonary endothelial inflammation and may lead to primary graft dysfunction (PGD). PGD is a significant cause of morbidity and mortality post-LTx. Research into preservation strategies that decrease the risk of LIRI and PGD is needed, and ex-situ lung perfusion (ESLP) is the foremost technological advancement in this field. This review addresses three major topics in the field of LTx: first, we review the clinical manifestation of LIRI post-LTx; second, we discuss the pathophysiology of LIRI that leads to pulmonary endothelial inflammation and PGD; and third, we present the role of ESLP as a therapeutic vehicle to mitigate this physiologic insult, increase the rates of donor organ utilization, and improve patient outcomes.
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Renteria, L. S., E. Cruz, and B. O. Ibe. "Platelet-activating factor synthesis and receptor-mediated signaling are downregulated in ovine newborn lungs: relevance in postnatal pulmonary adaptation and persistent pulmonary hypertension of the newborn." Journal of Developmental Origins of Health and Disease 4, no. 6 (July 22, 2013): 458–69. http://dx.doi.org/10.1017/s2040174413000366.
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Platelet-activating factor (PAF) is a phospholipid with a wide range of biological activities. We studied PAF metabolism and PAF receptor (PAFR) signaling in perinatal ovine lungs to understand PAF's role in transition of the perinatal pulmonary hemodynamics and pathophysiology of persistent pulmonary hypertension of the newborn. We hypothesized that downregulation of PAF synthesis with upregulation of PAF catabolism by acetylhydrolase (PAF-Ah) in the newborn lung is needed for fetus-to-newborn pulmonary adaptation. Studies were conducted on fetal and newborn lamb pulmonary arteries (PA), veins (PV) and smooth muscle cells (SMC). PAF metabolism, PAFR binding and cell proliferation were studied by cell culture; gene expression was studied by qPCR. Fetal lungs synthesized 60% more PAF than newborn lungs. Compared with the fetal PVs and SMCs, PAF-Ah activity in newborn was 40–60% greater. PAF-Ah mRNA expression in newborn vessels was different from the expression by fetal PA. PAF-Ah gene clone activity confirmed deletion of hypoxia-sensitive site. PAFR mRNA expression by the PVs and SMC-PV of the fetus and newborn was greater than by corresponding PAs and SMC-PA. Q-PCR study of PAFR expression by the SMC-PV of both groups was greater than SMC-PA. Fetal SMCs bound more PAF than the newborn SMCs. PAFR antagonist, CV-3988, inhibited PAFR binding and DNA synthesis by the fetal SMCs, but augmented binding and DNA synthesis by newborn cells. We show different PAF–PAFR mediated effects in perinatal lungs, suggesting both transcriptional and translational regulation of PAF-Ah and PAFR expression in the perinatal lamb lungs. These indicate that the downregulation of PAF-mediated effects postnatally protects against persistent pulmonary hypertension of the newborn.
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Lilburn, David M. L., Clémentine Lesbats, Joseph S. Six, Eric Dubuis, Liang Yew-Booth, Dominick E. Shaw, Maria G. Belvisi, Mark A. Birrell, Galina E. Pavlovskaya, and Thomas Meersmann. "Hyperpolarized 83 Kr magnetic resonance imaging of alveolar degradation in a rat model of emphysema." Journal of The Royal Society Interface 12, no. 107 (June 2015): 20150192. http://dx.doi.org/10.1098/rsif.2015.0192.
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Hyperpolarized 83 Kr surface quadrupolar relaxation (SQUARE) generates MRI contrast that was previously shown to correlate with surface-to-volume ratios in porous model surface systems. The underlying physics of SQUARE contrast is conceptually different from any other current MRI methodology as the method uses the nuclear electric properties of the spin I = 9/2 isotope 83 Kr. To explore the usage of this non-radioactive isotope for pulmonary pathophysiology, MRI SQUARE contrast was acquired in excised rat lungs obtained from an elastase-induced model of emphysema. A significant 83 Kr T 1 relaxation time increase in the SQUARE contrast was found in the elastase-treated lungs compared with the baseline data from control lungs. The SQUARE contrast suggests a reduction in pulmonary surface-to-volume ratio in the emphysema model that was validated by histology. The finding supports usage of 83 Kr SQUARE as a new biomarker for surface-to-volume ratio changes in emphysema.
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Hsia, Connie C. W., and Merryn H. Tawhai. "What can imaging tell us about physiology? Lung growth and regional mechanical strain." Journal of Applied Physiology 113, no. 6 (September 15, 2012): 937–46. http://dx.doi.org/10.1152/japplphysiol.00289.2012.
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The interplay of mechanical forces transduces diverse physico-biochemical processes to influence lung morphogenesis, growth, maturation, remodeling and repair. Because tissue stress is difficult to measure in vivo, mechano-sensitive responses are commonly inferred from global changes in lung volume, shape, or compliance and correlated with structural changes in tissue blocks sampled from postmortem-fixed lungs. Recent advances in noninvasive volumetric imaging technology, nonrigid image registration, and deformation analysis provide valuable tools for the quantitative analysis of in vivo regional anatomy and air and tissue-blood distributions and when combined with transpulmonary pressure measurements, allow characterization of regional mechanical function, e.g., displacement, strain, shear, within and among intact lobes, as well as between the lung and the components of its container—rib cage, diaphragm, and mediastinum—thereby yielding new insights into the inter-related metrics of mechanical stress-strain and growth/remodeling. Here, we review the state-of-the-art imaging applications for mapping asymmetric heterogeneous physical interactions within the thorax and how these interactions permit as well as constrain lung growth, remodeling, and compensation during development and following pneumonectomy to illustrate how advanced imaging could facilitate the understanding of physiology and pathophysiology. Functional imaging promises to facilitate the formulation of realistic computational models of lung growth that integrate mechano-sensitive events over multiple spatial and temporal scales to accurately describe in vivo physiology and pathophysiology. Improved computational models in turn could enhance our ability to predict regional as well as global responses to experimental and therapeutic interventions.
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Høy Marbjerg, Lis, Christina Jacobsen, Jannik Fonager, Claus Bøgelund, Morten Rasmussen, Anders Fomsgaard, Jytte Banner, and Veronika Vorobieva Solholm Jensen. "Possible Involvement of Central Nervous System in COVID-19 and Sequence Variability of SARS-CoV-2 Revealed in Autopsy Tissue Samples: A Case Report." Clinical Pathology 14 (January 2021): 2632010X2110060. http://dx.doi.org/10.1177/2632010x211006096.
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The case presented here illustrates that interdisciplinary teamwork can be essential for the understanding of the COVID-19 disease presentation and enlightening of the pathophysiology. A 60-year-old woman without any comorbidities, apart from overweight, was found dead in her apartment after 14 days of home isolation due to suspicion of COVID-19. A forensic autopsy was performed. This revealed severely condensed, almost airless, firm lungs, and the cause of death was severe acute respiratory distress syndrome-associated with COVID-19 (SARS-CoV-2). In addition, SARS-CoV-2 was detected with reverse transcription polymerase chain reaction (RT-PCR) in cerebrospinal fluid, lung tissue, and tracheal sample and specific antibodies for SARS-CoV-2 were detected in cerebrospinal fluid and serum. Subsequent sequencing of the SARS-CoV-2 virus showed variation in nucleotides at 3 sites between SARS-CoV-2 isolates recovered from the tracheal sample, cerebrospinal fluid, and tissues from both lungs, and phylogenetic analysis revealed that the spinal fluid sample differed the most from the other 3 samples. This case supports the hypothesis that SARS-CoV-2 may be neuroinvasive and cause central nervous system infection.
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Shrivastava, Bijal M., Kunal Kumar Jaiswal, Siddharth Budhreja, and Abhinav Tiwari. "Home environmental fungus: the hidden killer." International Journal of Contemporary Pediatrics 5, no. 2 (February 22, 2018): 667. http://dx.doi.org/10.18203/2349-3291.ijcp20180578.
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Hypersensitivity pneumonitis is generally attributed to inhalational organic dust, commonly due to exposure to dust at occupation or hobbies. Hypersensitivity pneumonitis or extrinsic allergic alveolitis is an inflammatory syndrome of lungs resulting from immunologically induced inflammation secondary to various airborne allergens. It is relatively rare in childhood. Knowledge of classical HRCT finding of lungs and use of antigen specific IgG and IgM antibodies (despite the false positive and false negative) analysis can act as supportive evidence for making diagnosis of Hypersensitivity pneumonitis. We report a case of 4 yrs old girl child who despite being symptomatic, remained undiagnosed for 18-24 months, was on bronchodilator therapy suspecting pathophysiology being Hyperreactive airway disease but had recurrent episodes. When her hypoxic condition worsened later on, she was further investigated to rule out other differential, HRCT done was suggestive of childhood interstitial lung disease. The allergens test done for aspergillus species was positive in home environment and in her blood. She responded to steroids therapy and removal of offending agents from home environment. This case shows the importance of home environment in causing life threatening respiratory disease in children. She was diagnosed with Hypersensitivity pneumonitis, rare in childhood.
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OBERT, MARTIN, STEFANIE HAGNER, GABRIELE A. KROMBACH, SELCUK INAN, and HARALD RENZ. "FRACTAL GEOMETRY ENABLES CLASSIFICATION OF DIFFERENT LUNG MORPHOLOGIES IN A MODEL OF EXPERIMENTAL ASTHMA." Fractals 23, no. 03 (July 31, 2015): 1550024. http://dx.doi.org/10.1142/s0218348x15500243.
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Animal models represent the basis of our current understanding of the pathophysiology of asthma and are of central importance in the preclinical development of drug therapies. The characterization of irregular lung shapes is a major issue in radiological imaging of mice in these models. The aim of this study was to find out whether differences in lung morphology can be described by fractal geometry. Healthy and asthmatic mouse groups, before and after an acute asthma attack induced by methacholine, were studied. In vivo flat-panel-based high-resolution Computed Tomography (CT) was used for mice's thorax imaging. The digital image data of the mice's lungs were segmented from the surrounding tissue. After that, the lungs were divided by image gray-level thresholds into two additional subsets. One subset contained basically the air transporting bronchial system. The other subset corresponds mainly to the blood vessel system. We estimated the fractal dimension of all sets of the different mouse groups using the mass radius relation (mrr). We found that the air transporting subset of the bronchial lung tissue enables a complete and significant differentiation between all four mouse groups (mean D of control mice before methacholine treatment: 2.64 ± 0.06; after treatment: 2.76 ± 0.03; asthma mice before methacholine treatment: 2.37 ± 0.16; after treatment: 2.71 ± 0.03; p < 0.05). We conclude that the concept of fractal geometry allows a well-defined, quantitative numerical and objective differentiation of lung shapes — applicable most likely also in human asthma diagnostics.
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Shiri Aghbash, Parisa, Hamed Ebrahimzadeh Leylabadlo, Hamidreza Fathi, Mohaddeseh Bahmani, Rojin Chegini, and Hossein Bannazadeh Baghi. "Hepatic Disorders and COVID-19: From Pathophysiology to Treatment Strategy." Canadian Journal of Gastroenterology and Hepatology 2022 (December 8, 2022): 1–15. http://dx.doi.org/10.1155/2022/4291758.
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Following the SARS-CoV-2 outbreak and the subsequent development of the COVID-19 pandemic, organs such as the lungs, kidneys, liver, heart, and brain have been identified as priority organs. Liver diseases are considered a risk factor for high mortality from the COVID-19 pandemic. Besides, liver damage has been demonstrated in a substantial proportion of patients with COVID-19, especially those with severe clinical symptoms. Furthermore, antiviral medications, immunosuppressive drugs after liver transplantation, pre-existing hepatic diseases, and chronic liver diseases such as cirrhosis have also been implicated in SARS-CoV-2-induced liver injury. As a result, some precautions have been taken to prevent, monitor the virus, and avoid immunocompromised and susceptible individuals, such as liver and kidney transplant recipients, from being infected with SARS-CoV-2, thereby avoiding an increase in mortality. The purpose of this review was to examine the impairment caused by SARS-CoV-2 infection and the impact of drugs used during the pandemic on the mortality range and therefore the possibility of preventive measures in patients with liver disease.