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Articoli di riviste sul tema "Lungs Inflammation"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 27 gennaio 2023

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1

Kumar, Rajiv. "SARS-CoV-2, Inflammation, Allergy of the Lungs and Nanotherapeutics." International Journal of Clinical Case Reports and Reviews 11, no. 1 (April 4, 2022): 01–02. http://dx.doi.org/10.31579/2690-4861/208.

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Nanomaterials and nanotechnology are quite helpful in disease identification, prevention, treatment, scheming, and monitoring [4]. The properties of multifunctional nanomaterials altered by applying the strategies of nanotechnology and furnished for designing novel remedies for various medical applications. Furthermore, modified features of nanomaterials can influence their fate and also upgrade their claims in inhalation. Thus these types of nanoscale innovations achieved by adopting aforesaid strategies significantly. The nanotools and remedies treat viral infection and, in the end, also imp

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2

Le, Nguyen Phuong Khanh, Shankaramurthy Channabasappa, Mokarram Hossain, Lixin Liu, and Baljit Singh. "Leukocyte-specific protein 1 regulates neutrophil recruitment in acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 9 (November 1, 2015): L995—L1008. http://dx.doi.org/10.1152/ajplung.00068.2014.

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The mechanisms of excessive migration of activated neutrophils into inflamed lungs, credited with tissue damage, are not fully understood. We explored the hitherto unknown expression of leukocyte-specific protein 1 (LSP1) in human and mouse lungs and neutrophils and examined its role in neutrophil migration in acute lung inflammation. Autopsied septic human lungs showed increased LSP1 labeling in epithelium, endothelium, and leukocytes, including in their nuclei compared with normal lungs. We induced acute lung inflammation through intranasal administration of E. coli lipopolysaccharide (LPS)

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3

Lorenzo, Erica, Jacob Hopkins, Julie Lefebvre, and Laura Haynes. "Vaccination does not protect aged mice from influenza-induced lung inflammation (VAC9P.1062)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 145.2. http://dx.doi.org/10.4049/jimmunol.194.supp.145.2.

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Abstract Aging predisposes individuals to increased susceptibility to influenza infection and delays in viral clearance. Importantly, we show that age-related delays in viral clearance are correlated with lingering inflammation in the lungs of aged mice. This is critical since inflammation in the lungs is associated with an enhanced susceptibility to secondary bacterial infection, which is a significant sequela to flu infection and often causes death. Inflammation in young lungs following flu infection can be significantly reduced by prior flu immunity, such as that generated following vaccina

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4

Small, Donna M., Ryan R. Brown, Declan F. Doherty, Anthony Abladey, Zhe Zhou-Suckow, Rebecca J. Delaney, Lauren Kerrigan, et al. "Targeting of cathepsin S reduces cystic fibrosis-like lung disease." European Respiratory Journal 53, no. 3 (January 17, 2019): 1801523. http://dx.doi.org/10.1183/13993003.01523-2018.

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Cathepsin S (CatS) is upregulated in the lungs of patients with cystic fibrosis (CF). However, its role in CF lung disease pathogenesis remains unclear.In this study, β-epithelial Na+ channel-overexpressing transgenic (βENaC-Tg) mice, a model of CF-like lung disease, were crossed with CatS null (CatS−/−) mice or treated with the CatS inhibitor VBY-999.Levels of active CatS were elevated in the lungs of βENaC-Tg mice compared with wild-type (WT) littermates. CatS−/−βENaC-Tg mice exhibited decreased pulmonary inflammation, mucus obstruction and structural lung damage compared with βENaC-Tg mice.

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5

Ramos-Ramírez, Patricia, Carina Malmhäll, Kristina Johansson, Mikael Adner, Jan Lötvall, and Apostolos Bossios. "Lung Regulatory T Cells Express Adiponectin Receptor 1: Modulation by Obesity and Airway Allergic Inflammation." International Journal of Molecular Sciences 21, no. 23 (November 26, 2020): 8990. http://dx.doi.org/10.3390/ijms21238990.

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Regulatory T cells (Tregs) decrease in the adipose tissue upon weight gain, contributing to persistent low-grade inflammation in obesity. We previously showed that adipose tissue Tregs express the adiponectin receptor 1 (AdipoR1); however, the expression in lung Tregs is still unknown. Here, we aimed to determine whether Helios+ and Helios− Treg subsets expressed AdipoR1 in the lungs of obese mice and whether different obesity grades affected the expression upon allergic lung inflammation. For diet-induced obesity (DIO), mice were fed a high-fat diet (HFD) for up to 15 weeks (overweight), 21 w

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6

Chapoval, Svetlana P., Ann E. Kelly-Welch, Elizabeth Smith, and Achsah D. Keegan. "Complex role of STAT6 in allergic airway inflammation (39.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S27. http://dx.doi.org/10.4049/jimmunol.178.supp.39.11.

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Abstract STAT6 plays a critical role in Th2 cell differentiation and in allergic lung inflammation. Using a chimeric mouse model, we observed alternative lung pathology in STAT6 KO mice even when WT bone marrow or Th2 cells were provided. Thus, we hypothesized that STAT6 contributes to inflammation in a complex manner. To detail STAT6 function, WT and STAT6 KO mice were subjected to OVA priming and challenges. Broncho-alveolar lavage (BAL) cell composition, lung histology, and FACS analysis of digested lungs were assessed 48h after the last challenge. As expected, eosinophils composed a majori

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7

Herbein, Joel F., and Jo Rae Wright. "Enhanced clearance of surfactant protein D during LPS-induced acute inflammation in rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 1 (July 1, 2001): L268—L277. http://dx.doi.org/10.1152/ajplung.2001.281.1.l268.

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Pulmonary surfactant participates in the regulation of alveolar compliance and lung host defense. Surfactant homeostasis is regulated through a combination of synthesis, secretion, clearance, recycling, and degradation of surfactant components. The extracellular pool size of surfactant protein (SP) D fluctuates significantly during acute inflammation. We hypothesized that changes in SP-D levels are due, in part, to altered clearance of SP-D. Clearance pathways in rats were assessed with fluorescently labeled SP-D that was instilled into control lungs or lungs that had been treated with lipopol

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8

Ahn, So Yoon, Dong Kyung Sung, Yun Sil Chang, and Won Soon Park. "Intratracheal Transplantation of Mesenchymal Stem Cells Attenuates Hyperoxia-Induced Microbial Dysbiosis in the Lungs, Brain, and Gut in Newborn Rats." International Journal of Molecular Sciences 23, no. 12 (June 13, 2022): 6601. http://dx.doi.org/10.3390/ijms23126601.

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We attempted to determine whether intratracheal (IT) transplantation of mesenchymal stem cells (MSCs) could simultaneously attenuate hyperoxia-induced lung injuries and microbial dysbiosis of the lungs, brain, and gut in newborn rats. Newborn rats were exposed to hyperoxia (90% oxygen) for 14 days. Human umbilical cord blood-derived MSCs (5 × 105) were transplanted via the IT route on postnatal day (P) five. At P14, the lungs were harvested for histological, biochemical, and microbiome analyses. Bacterial 16S ribosomal RNA genes from the lungs, brain, and large intestine were amplified, pyrose

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9

Marín-Corral, Judith, Leticia Martínez-Caro, José A. Lorente, Marta de Paula, Lara Pijuan, Nicolas Nin, Joaquim Gea, Andrés Esteban, and Esther Barreiro. "Redox Balance and Cellular Inflammation in the Diaphragm, Limb Muscles, and Lungs of Mechanically Ventilated Rats." Anesthesiology 112, no. 2 (February 1, 2010): 384–94. http://dx.doi.org/10.1097/aln.0b013e3181c38bed.

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Background High tidal volume (VT) mechanical ventilation was shown to induce organ injury other than lung injury and systemic inflammation in animal models of ventilator-induced lung injury. The authors aimed to explore whether high VT mechanical ventilation per se induces early oxidative stress and inflammation in the diaphragm, limb muscles, and lungs of healthy rats exposed to ventilator-induced lung injury. Methods Protein carbonylation and nitration, antioxidants (immunoblotting), and inflammation (immunohistochemistry) were evaluated in the diaphragm, gastrocnemius, soleus, tibialis ante

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10

Bai, Jing, Shi-Lin Qiu, Xiao-Ning Zhong, Qiu-Ping Huang, Zhi-Yi He, Jian-Quan Zhang, Guang-Nan Liu, Mei-Hua Li, and Jing-Min Deng. "Erythromycin EnhancesCD4+Foxp3+Regulatory T-Cell Responses in a Rat Model of Smoke-Induced Lung Inflammation." Mediators of Inflammation 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/410232.

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Heavy smoking can induce airway inflammation and emphysema. Macrolides can modulate inflammation and effector T-cell response in the lungs. However, there is no information on whether erythromycin can modulate regulatory T-cell (Treg) response. This study is aimed at examining the impact of erythromycin on Treg response in the lungs in a rat model of smoking-induced emphysema. Male Wistar rats were exposed to normal air or cigarette smoking daily for 12 weeks and treated by gavage with 100 mg/kg of erythromycin or saline daily beginning at the forth week for nine weeks. The lung inflammation a

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11

Markovic, N., L. A. McCaig, J. Stephen, S. Mizuguchi, R. A. W. Veldhuizen, J. F. Lewis, and G. Cepinskas. "Mediators released from LPS-challenged lungs induce inflammatory responses in liver vascular endothelial cells and neutrophilic leukocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 6 (December 2009): G1066—G1076. http://dx.doi.org/10.1152/ajpgi.00278.2009.

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The systemic inflammatory response plays an important role in the progression of acute lung injury (ALI) to multiple organ dysfunction syndrome (MODS). However, the role of lung-derived inflammatory mediators in induction of the inflammatory response in remote organs is poorly understood. To address the above, we investigated the effects of lung inflammation on induction of inflammatory response(s) in the liver in vitro. Inflammation in mouse lungs was induced by intranasal administration of lipopolysaccharide (LPS; 1 mg/ml) followed by mechanical ventilation using the isolated perfused mouse

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12

de Prost, Nicolas, Eduardo L. Costa, Tyler Wellman, Guido Musch, Tilo Winkler, Mauro R. Tucci, R. Scott Harris, Jose G. Venegas, and Marcos F. Vidal Melo. "Effects of surfactant depletion on regional pulmonary metabolic activity during mechanical ventilation." Journal of Applied Physiology 111, no. 5 (November 2011): 1249–58. http://dx.doi.org/10.1152/japplphysiol.00311.2011.

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Inflammation during mechanical ventilation is thought to depend on regional mechanical stress. This can be produced by concentration of stresses and cyclic recruitment in low-aeration dependent lung. Positron emission tomography (PET) with 18F-fluorodeoxyglucose (18F-FDG) allows for noninvasive assessment of regional metabolic activity, an index of neutrophilic inflammation. We tested the hypothesis that, during mechanical ventilation, surfactant-depleted low-aeration lung regions present increased regional 18F-FDG uptake suggestive of in vivo increased regional metabolic activity and inflamma

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13

Goenharto, Sianiwati, I. Ketut Sudiana, Sherman Salim, Elly Rusdiana, and Sri Wahjuni. "Inflammation in the lungs of mice due to methyl methacrylate exposure." February-2020 13, no. 2 (2020): 256–60. http://dx.doi.org/10.14202/vetworld.2020.256-260.

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Aim: This study aimed to predict the potential inflammation in lungs caused by exposure to methyl methacrylate (MMA; in silico study) and assess inflammation in lungs in response to MMA inhalation in mice (in vivo study). Materials and Methods: In silico and in vivo studies were performed using 24 mice divided into a control group (0 ppm MMA) and five treatment groups, which were exposed to 150 ppm MMA for 40, 80, 120, 160, and 200 min, respectively. Lung tissues were harvested and examined with a light microscope at 400×. Results: In silico studies confirmed the existence of one activation bo

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14

Vrolyk, V., B. K. Wobeser, A. N. Al-Dissi, A. Carr, and B. Singh. "Lung Inflammation Associated With Clinical Acute Necrotizing Pancreatitis in Dogs." Veterinary Pathology 54, no. 1 (September 30, 2016): 129–40. http://dx.doi.org/10.1177/0300985816646432.

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Although dogs with acute necrotizing pancreatitis (ANP) can develop respiratory complications, there are no data describing lung injury in clinical cases of ANP in dogs. Therefore, we conducted a study to characterize lung injury and determine if pulmonary intravascular macrophages (PIMs) are induced in dogs with ANP ( n = 21) compared with control dogs ( n = 6). Two pathologists independently graded histologic sections of pancreas from clinical cases to characterize the severity of ANP (total scores of 3–10) compared with controls showing histologically normal pancreas (total scores of 0). Ba

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15

Babić, Rade, Gordana Stanković-Babić, Strahinja Babić, Aleksandra Marjanović, Nenad Govedarović, and Nevena Babić. "X-ray aspects of lung inflammation COVID-19." Medicinska rec 1, no. 3 (2020): 127–35. http://dx.doi.org/10.5937/medrec2003127b.

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Coronavirus disease 2019 (COVID-19) is a severe infectious disease of the respiratory system with clinical signs of severe acute respiratory syndrome. The causative agent is coronavirus 2 (SARS-CoV-2). Common symptoms of COVID-19 pneumonia are fever, cough, shortness of breath, myalgia, expectoration of sputum and sore throat. The X-ray image of COVID-19 pneumonia has its own characteristics and changes with the evolution of the disease. At the beginning of the disease, the radiological finding in the lungs may be normal or changes may be visualized in the lungs in the form of multiple hazy va

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Sadykova, Gulora A., Kh U. Rakhmatullaev, R. Sh Mavlyan-Khodjaev, Z. S. Zalyalova, and Yu Kh Tadjikhodjaeva. "THE INFLUENCE OF OZONE THERAPY ON THE MORPHOLOGIC CHANGES IN THE PATIENTS PRESENTING WITH PURULENT INFLAMMATION OF THE LUNGS IN THE EXPERIMENT." Russian Journal of Physiotherapy, Balneology and Rehabilitation 16, no. 3 (June 15, 2017): 137–40. http://dx.doi.org/10.18821/1681-3456-2017-16-3-137-140.

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We have created the experimental model of chronic inflammation of lungs by means of prolonged mechanical irritation of the bronchi in 30 outbred rats and studied the morphological changes in the lung tissue of these animals rats in three series of experiments. Each rat was given an intraperitoneal injection of an ozonised saline solution produced by a «Binafsha» ozonator. The objective of the study was to compare a control group of healthy animals and the group of experimental animals with chronic purulent pneumonia. The prolonged irritation of the respiratory tract in experimental animals was

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17

Locke, Landon W., Mark B. Williams, Karen D. Fairchild, Min Zhong, Bijoy K. Kundu, and Stuart S. Berr. "FDG-PET Quantification of Lung Inflammation with Image-Derived Blood Input Function in Mice." International Journal of Molecular Imaging 2011 (December 10, 2011): 1–6. http://dx.doi.org/10.1155/2011/356730.

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Dynamic FDG-PET imaging was used to study inflammation in lungs of mice following administration of a virulent strain of Klebsiella (K.) pneumoniae. Net whole-lung FDG influx constant (Ki) was determined in a compartment model using an image-derived blood input function. Methods. K. pneumoniae (~3 x 105 CFU) was intratracheally administered to six mice with 6 other mice serving as controls. Dynamic FDG-PET and X-Ray CT scans were acquired 24 hr after K. pneumoniae administration. The experimental lung time activity curves were fitted to a 3-compartment FDG model to obtain Ki. Following imaging

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18

Savin, Innokenty A., Marina A. Zenkova, and Aleksandra V. Sen’kova. "Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches." International Journal of Molecular Sciences 23, no. 23 (November 29, 2022): 14959. http://dx.doi.org/10.3390/ijms232314959.

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Pulmonary fibrosis is a chronic progressive lung disease that steadily leads to lung architecture disruption and respiratory failure. The development of pulmonary fibrosis is mostly the result of previous acute lung inflammation, caused by a wide variety of etiological factors, not resolved over time and causing the deposition of fibrotic tissue in the lungs. Despite a long history of study and good coverage of the problem in the scientific literature, the effective therapeutic approaches for pulmonary fibrosis treatment are currently lacking. Thus, the study of the molecular mechanisms underl

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Wilson, Carole L., Chi F. Hung, and Lynn M. Schnapp. "Endotoxin-induced acute lung injury in mice with postnatal deletion of nephronectin." PLOS ONE 17, no. 5 (May 12, 2022): e0268398. http://dx.doi.org/10.1371/journal.pone.0268398.

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Acute injury of the lung involves damage to the epithelium and its underlying extracellular matrix (ECM), the basement membrane (BM). How BMs contribute to injury resolution is poorly understood. Nephronectin (NPNT) is a high-affinity ligand for integrin α8β1 and, although first identified in the mouse kidney, is prominently expressed in the lung, where it localizes to BMs in the alveoli. To determine if NPNT plays a role in acute injury and inflammation of the lung, we developed a model for postnatal deletion of NPNT using mice with a floxed allele of Npnt in combination with a tamoxifen-indu

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Thatcher, T. H., N. A. McHugh, R. W. Egan, R. W. Chapman, J. A. Hey, C. K. Turner, M. R. Redonnet, K. E. Seweryniak, P. J. Sime, and R. P. Phipps. "Role of CXCR2 in cigarette smoke-induced lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 2 (August 2005): L322—L328. http://dx.doi.org/10.1152/ajplung.00039.2005.

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It has been hypothesized that the destruction of lung tissue observed in smokers with chronic obstructive pulmonary disease and emphysema is mediated by neutrophils recruited to the lungs by smoke exposure. This study investigated the role of the chemokine receptor CXCR2 in mediating neutrophilic inflammation in the lungs of mice acutely exposed to cigarette smoke. Exposure to dilute mainstream cigarette smoke for 1 h, twice per day for 3 days, induced acute inflammation in the lungs of C57BL/6 mice, with increased neutrophils and the neutrophil chemotactic CXC chemokines macrophage inflammato

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Cohen, Pazit Y., Raphael Breuer, Philip Zisman, and Shulamit B. Wallach-Dayan. "Bleomycin-Treated Chimeric Thy1-Deficient Mice with Thy1-Deficient Myofibroblasts and Thy-Positive Lymphocytes Resolve Inflammation without Affecting the Fibrotic Response." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/942179.

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Lung fibrosis is characterized by abnormal accumulation of fibroblasts in the interstitium of the alveolar space. Two populations of myofibroblasts, distinguished by Thy1 expression, are detected in human and murine lungs. Accumulation of Thy1-negative (Thy1−) myofibroblasts was shown in the lungs of humans with idiopathic pulmonary fibrosis (IPF) and of bleomycin-treated mice. We aimed to identify genetic changes in lung myofibroblasts following Thy1 crosslinking and assess the impact of specific lung myofibroblast Thy1-deficiency, in vivo, in bleomycin-injured mouse lungs. Thy1 increased in

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Fales-Williams, A. J., K. A. Brogden, E. Huffman, J. M. Gallup, and M. R. Ackermann. "Cellular Distribution of Anionic Antimicrobial Peptide in Normal Lung and during Acute Pulmonary Inflammation." Veterinary Pathology 39, no. 6 (November 2002): 706–11. http://dx.doi.org/10.1354/vp.39-6-706.

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Anionic peptides (APs) are small antimicrobial peptides present in human and ovine lung. In this study APs were also detected in bovine lung, and production of APs in lungs with acute inflammation induced by various stimuli was determined. The distribution and intensity of APs were determined by immunohistochemistry in lungs of 1) neonatal calves (1-3 days of age) inoculated with Mannheimia (Pasteurella) haemolytica, a known inducer of the bovine β-defensin lingual antimicrobial peptide (LAP) or pyrogen-free saline (PFS), and 2) growing calves (3 months of age) similarly inoculated with M. hae

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Léger, Caroline, Ai Ni, Graciela Andonegui, Josée Wong, Connie Mowat, and Brent W. Winston. "Adenovirus-mediated gene transfer of hIGF-IB in mouse lungs induced prolonged inflammation but no fibroproliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 4 (April 2010): L492—L500. http://dx.doi.org/10.1152/ajplung.00310.2009.

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Pulmonary fibrosis (PF), the end stage of a variety of fibroproliferative lung diseases, is characterized by excessive lung mesenchymal cell activation and extracellular matrix deposition. Most PF is induced after repetitive or chronic lung inflammation; however, a significant portion of PF occurs without apparent inflammation. The mechanisms of fibroproliferation are poorly understood. Studies have shown that cytokines regulating inflammation and tissue repair processes play essential roles in the development of PF. Insulin-like growth factor I (IGF-I) has been shown to stimulate lung mesench

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Duong, Chi, Huei Jiunn Seow, Steven Bozinovski, Peter J. Crack, Gary P. Anderson, and Ross Vlahos. "Glutathione peroxidase-1 protects against cigarette smoke-induced lung inflammation in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 299, no. 3 (September 2010): L425—L433. http://dx.doi.org/10.1152/ajplung.00038.2010.

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Reactive oxygen species (ROS) produced from cigarette smoke cause oxidative lung damage including protein denaturation, lipid peroxidation, and DNA damage. Glutathione peroxidase-1 (gpx-1) is a detoxifying enzyme that may protect lungs from such damage. The aim of this study was to determine whether gpx-1 protects the lung against oxidative stress-induced lung inflammation in vivo. Male wild-type (WT) or gpx-1−/− mice were exposed to cigarette smoke generated from nine cigarettes per day for 4 days to induce oxidative stress and lung inflammation. The effect of the gpx mimetic ebselen on cigar

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Lagasse, H. A. Daniel, and Alan Scott. "Lung macrophages control malaria-induced pulmonary inflammation (56.17)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 56.17. http://dx.doi.org/10.4049/jimmunol.186.supp.56.17.

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Abstract Pulmonary edema and acute respiratory distress are archetypal symptoms of severe malaria that occur in ~20% of patients and are associated with mortality rates exceeding 70%. Little is known about the pathogenesis of lung pathology associated with Plasmodium infections. We tested the hypothesis that two major cellular populations - CD11c+CD11b- resident macrophages and CD11b+Ly6C+ recruited monocytes/macrophages - are key players in regulating the nature and magnitude of malaria-induced pulmonary pathology. During the very early stages of Plasmodium berghei infections in mice, parasit

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Wang, Ping, Lin Zhang, Yanxia Liao, Juan Du, Mengying Xu, Wen Zhao, Shuxian Yin, et al. "Effect of Intratracheal Instillation of ZnO Nanoparticles on Acute Lung Inflammation Induced by Lipopolysaccharides in Mice." Toxicological Sciences 173, no. 2 (December 5, 2019): 373–86. http://dx.doi.org/10.1093/toxsci/kfz234.

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Abstract Although studies have shown toxic effects of zinc oxide (ZnO) particles following inhalation, additional effects on injured lungs, which are characterized by dysfunction of the alveolar-capillary barriers, remain uncharacterized. To explore these additional effects, nano-sized ZnO (nZnO) and bulk-sized ZnO were applied to lipopolysaccharide (LPS)-challenged mouse lungs, which were used as a disease model of acute lung inflammation. An elevated Zn2+ concentration was detected in lung tissue after LPS plus nZnO exposure. Exposure to nZnO in LPS-challenged mice resulted in higher total c

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Hogmalm, Anna, Maija Bry та Kristina Bry. "Pulmonary IL-1β expression in early life causes permanent changes in lung structure and function in adulthood". American Journal of Physiology-Lung Cellular and Molecular Physiology 314, № 6 (1 червня 2018): L936—L945. http://dx.doi.org/10.1152/ajplung.00256.2017.

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Chorioamnionitis, mechanical ventilation, oxygen therapy, and postnatal infection promote inflammation in the newborn lung. The long-term consequences of pulmonary inflammation during infancy have not been well characterized. The aim of this study was to examine the impact of inflammation during the late saccular to alveolar stages of lung development on lung structure and function in adulthood. To induce IL-1β expression in the pulmonary epithelium of mice with a tetracycline-inducible human IL-1β transgene, doxycycline was administered via intraperitoneal injections to bitransgenic pups and

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Hellman, Urban, Mats G. Karlsson, Anna Engström-Laurent, Sara Cajander, Luiza Dorofte, Clas Ahlm, Claude Laurent, and Anders Blomberg. "Presence of hyaluronan in lung alveoli in severe Covid-19: An opening for new treatment options?" Journal of Biological Chemistry 295, no. 45 (September 25, 2020): 15418–22. http://dx.doi.org/10.1074/jbc.ac120.015967.

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Severe coronavirus disease 2019 (Covid-19) is characterized by inflammation of the lungs with increasing respiratory impairment. In fatal Covid-19, lungs at autopsy have been filled with a clear liquid jelly. However, the nature of this finding has not yet been determined. The aim of the study was to demonstrate whether the lungs of fatal Covid-19 contain hyaluronan, as it is associated with inflammation and acute respiratory distress syndrome (ARDS) and may have the appearance of liquid jelly. Lung tissue obtained at autopsy from three deceased Covid-19 patients was processed for hyaluronan h

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Kunzmann, Steffen, Christian P. Speer, Alan H. Jobe та Boris W. Kramer. "Antenatal inflammation induced TGF-β1 but suppressed CTGF in preterm lungs". American Journal of Physiology-Lung Cellular and Molecular Physiology 292, № 1 (січень 2007): L223—L231. http://dx.doi.org/10.1152/ajplung.00159.2006.

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Chorioamnionitis is frequently associated with preterm birth and increases the risk of adverse outcomes such as bronchopulmonary dysplasia (BPD). Transforming growth factor (TGF)-β1 is a key regulator of lung development, airway remodeling, lung fibrosis, and regulation of inflammation, and all these processes contribute to the development of BPD. Connective tissue growth factor (CTGF) is a downstream mediator of some of the profibrotic effects of TGF-β1, vascular remodeling, and angiogenesis. TGF-β1-induced CTGF expression can be blocked by TNF-α. We asked whether chorioamnionitis-associated

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Zhang, Xinfu, Weiyu Zhao, Bin Li, Wenqing Li, Chengxiang Zhang, Xucheng Hou, Justin Jiang, and Yizhou Dong. "Ratiometric fluorescent probes for capturing endogenous hypochlorous acid in the lungs of mice." Chemical Science 9, no. 43 (2018): 8207–12. http://dx.doi.org/10.1039/c8sc03226b.

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Papinska, Joanna Aleksandra, Grzegorz Gmyrek, R. Sathish Srinivasan, Umesh Deshmukh, and Harini Bagavant. "Pulmonary involvement in a mouse model of Sjögren’s syndrome induced by activation of the STING pathway." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 180.16. http://dx.doi.org/10.4049/jimmunol.202.supp.180.16.

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Abstract Sjögren’s Syndrome (SS) is a chronic autoimmune disorder characterized by an increased type 1 interferon gene signature, autoantibody production, and salivary gland inflammation. Engagement of Stimulator of interferon genes (STING) induces type 1 interferon production. Gain of function mutations in TMEM173, encoding STING, results in a severe vasculopathy affecting the skin and lungs. We have previously reported that activation of the STING pathway in mice, using a STING agonist DMXAA, causes an SS-like disease characterized by sialoadenitis and salivary gland dysfunction. Considering

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Singh, Ram Raj, and Isela Valera. "Plasmacytoid dendritic cells contribute to pro-inflammatory and pro-fibrotic milieu in lung fibrosis." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 182.76. http://dx.doi.org/10.4049/jimmunol.202.supp.182.76.

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Abstract Fibrosis, the end-result of tissue injury in a wide range of diseases, contributes to &gt;40% of mortality in the US. Plasmacytoid dendritic cells (pDC) are reduced in the peripheral blood, but increase in the lungs and skin of patients with systemic sclerosis, a prototypic fibrotic disease (JCI Insight 2018). The frequency of pDCs in the lungs of patients correlated with the severity of lung disease and with levels of proteins implicated in inflammation and fibrosis. Importantly, depletion of pDCs ameliorated lung and skin fibrosis in the bleomycin-induced animal model. pDC deple

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Libreros, Stephania, Ramon Garcia-Areas, and Vijaya Iragavarapu. "Chitinase-3 like-protein-1 (CHI3L1) expression associated with pulmonary inflammation accelerates breast cancer metastasis (TUM7P.960)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 203.42. http://dx.doi.org/10.4049/jimmunol.192.supp.203.42.

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Abstract Disseminated metastasis accounts for a majority of breast cancer deaths. Recently, elevated serum levels of a glycoprotein known as chitinase-3 like-protein-1 (CHI3L1) has been correlated with poor prognosis in both breast cancer and asthmatic patients. We have combined mouse models of breast cancer and pulmonary inflammation to determine if CHI3L1 associated pulmonary inflammation accelerates metastasis. We found that allergic pulmonary inflammation significantly enhances primary tumor growth in 4T1, 4T07 and 67NR mammary tumors by 10-fold, while decreasing survival. 4T1 tumor bearer

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Hardwick, Matthew J., Ming-Kai Chen, Kwamena Baidoo, Martin G. Pomper, and Tomás R. Guilarte. "In Vivo Imaging of Peripheral Benzodiazepine Receptors in Mouse Lungs: A Biomarker of Inflammation." Molecular Imaging 4, no. 4 (October 1, 2005): 7290.2005.05133. http://dx.doi.org/10.2310/7290.2005.05133.

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The ability to visualize the immune response with radioligands targeted to immune cells will enhance our understanding of cellular responses in inflammatory diseases. Peripheral benzodiazepine receptors (PBR) are present in monocytes and neutrophils as well as in lung tissue. We used lipopolysaccharide (LPS) as a model of inflammation to assess whether the PBR could be used as a noninvasive marker of inflammation in the lungs. Planar imaging of mice administrated 10 or 30 mg/kg LPS showed increased [123I]-( R)-PK11195 radioactivity in the thorax 2 days after LPS treatment relative to control.

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Tjota, Melissa, та Anne Sperling. "Activation of monocytes through FcRγ-signaling promotes IL-33-dependent migration into the lung interstitium (HYP7P.270)". Journal of Immunology 194, № 1_Supplement (1 травня 2015): 191.18. http://dx.doi.org/10.4049/jimmunol.194.supp.191.18.

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Abstract The development of Type 2 responses, such as those seen in asthma, has been significantly associated with IL-33. Previously, we demonstrated that allergen-specific IgG immune complex (IC) signaling through FcγRIII on IL-33 sufficient DCs induced Type 2 allergic airway inflammation. These data suggested that IL-33-/- mice, which had diminished Type 2 responses in the lungs, had a defect in APC function. For this study, we focused on monocytes and CD11b+ monocyte-derived DCs (moDCs) as they were shown to have the highest levels of FcγRIII expression, antigen uptake, and IL-33 upregulati

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Vakhidova, A. M. "EFFICACY OF LYMPHOTROPIC ADMINISTRATION OF BACTOX (AMOXICILIN) IN THE TREATMENT OF CHRONIC PNEUMONIA IN CHILDREN." American Journal of Medical Sciences and Pharmaceutical Research 04, no. 02 (February 1, 2022): 4–6. http://dx.doi.org/10.37547/tajmspr/volume04issue02-02.

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Abstract (sommario):

Lung inflammation, also called pneumonia, is a pathological process that affects lung tissue. It occurs in both adults and children. Inflammation of the lungs needs urgent treatment, even if it is not severe. Pneumonia is mainly caused by an infection - an invasion of the lung by pathogenic organisms. Therefore, the use of antibiotics for pneumonia in adults and children, together with complementary medicines, is the mainstay of treatment.

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Woods, David F., Stephanie Flynn, Jose A. Caparrós-Martín, Stephen M. Stick, F. Jerry Reen, and Fergal O’Gara. "Systems Biology and Bile Acid Signalling in Microbiome-Host Interactions in the Cystic Fibrosis Lung." Antibiotics 10, no. 7 (June 24, 2021): 766. http://dx.doi.org/10.3390/antibiotics10070766.

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The study of the respiratory microbiota has revealed that the lungs of healthy and diseased individuals harbour distinct microbial communities. Imbalances in these communities can contribute to the pathogenesis of lung disease. How these imbalances occur and establish is largely unknown. This review is focused on the genetically inherited condition of Cystic Fibrosis (CF). Understanding the microbial and host-related factors that govern the establishment of chronic CF lung inflammation and pathogen colonisation is essential. Specifically, dissecting the interplay in the inflammation–pathogen–h

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Maehara, Toko, та Ko Fujimori. "Inhibition of Prostaglandin F2α Receptors Exaggerates HCl-Induced Lung Inflammation in Mice". International Journal of Molecular Sciences 22, № 23 (27 листопада 2021): 12843. http://dx.doi.org/10.3390/ijms222312843.

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe respiratory disorders that are caused by aspiration, sepsis, trauma, and pneumonia. A clinical feature of ALI/ARDS is the acute onset of severe hypoxemia, and the mortality rate, which is estimated at 38–50%, remains high. Although prostaglandins (PGs) are detected in the bronchoalveolar lavage fluid of patients with ALI/ARDS, the role of PGF2α in ALI remains unclear. We aimed to clarify the role of PGF2α/PGF2α receptor (FP) signaling in acid-induced ALI using an FP receptor antagonist, AL8810. Intratracheal inje

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Bajrami, Besnik, Haiyan Zhu, Hyun-Jeong Kwak, Subhanjan Mondal, Qingming Hou, Guangfeng Geng, Kutay Karatepe, et al. "G-CSF maintains controlled neutrophil mobilization during acute inflammation by negatively regulating CXCR2 signaling." Journal of Experimental Medicine 213, no. 10 (August 22, 2016): 1999–2018. http://dx.doi.org/10.1084/jem.20160393.

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Abstract (sommario):

Cytokine-induced neutrophil mobilization from the bone marrow to circulation is a critical event in acute inflammation, but how it is accurately controlled remains poorly understood. In this study, we report that CXCR2 ligands are responsible for rapid neutrophil mobilization during early-stage acute inflammation. Nevertheless, although serum CXCR2 ligand concentrations increased during inflammation, neutrophil mobilization slowed after an initial acute fast phase, suggesting a suppression of neutrophil response to CXCR2 ligands after the acute phase. We demonstrate that granulocyte colony-sti

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Abonia, J. Pablo, Jenny Hallgren, Tatiana Jones, Tong Shi, Yuhui Xu, Pandelakis Koni, Richard A. Flavell, Joshua A. Boyce, K. Frank Austen, and Michael F. Gurish. "Alpha-4 integrins and VCAM-1, but not MAdCAM-1, are essential for recruitment of mast cell progenitors to the inflamed lung." Blood 108, no. 5 (September 1, 2006): 1588–94. http://dx.doi.org/10.1182/blood-2005-12-012781.

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Abstract (sommario):

Normal mouse lungs lack appreciable numbers of mast cells (MCs) or MC progenitors (MCp's), yet the appearance of mature MCs in the tracheobronchial epithelial surface is a characteristic of allergic, T-cell-dependent pulmonary inflammation. We hypothesized that pulmonary inflammation would recruit MCp's to inflamed lungs and that this recruitment would be regulated by distinct adhesion pathways. Ovalbumin-sensitized and challenged mice had a greater than 28-fold increase in the number of MCp's in the lungs. In mice lacking endothelial vascular cell adhesion molecule 1 (VCAM-1) and in wild-type

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Hart, David A., Francis Green, Paul Whidden, Jack Henkin, and Donald E. Woods. "Exogenous rh-urokinase modifies inflammation and Pseudomonas aeruginosa infection in a rat chronic pulmonary infection model." Canadian Journal of Microbiology 39, no. 12 (December 1, 1993): 1127–34. http://dx.doi.org/10.1139/m93-170.

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Abstract (sommario):

The effect of recombinant human urokinase (rh-UK) in a rat model of chronic Pseudomonas aeruginosa pulmonary infection was studied. Efficacy was assessed by lung histology and quantitative bacteriology. Male Sprague–Dawley rats received 1 × 104 or 1 × 105P. aeruginosa encapsulated in agar beads via the intratracheal route on day 1. Intratracheal administration of up to 12 500 units of rh-UK on day 21 led to a dose-dependent disappearance of viable organisms from the lungs by day 24 in rats receiving 104 organisms. In slightly longer term infections (30 days), rh-UK was still effective in facil

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Wang, Qin, Jianchun Wang, Mingdong Hu, Yu Yang, Liang Guo, Jing Xu, Chuanjiang Lei, Yan Jiao, and JianCheng Xu. "Uncoupling Protein 2 Increases Susceptibility to Lipopolysaccharide-Induced Acute Lung Injury in Mice." Mediators of Inflammation 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/9154230.

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Abstract (sommario):

Uncoupling protein 2 (UCP2) is upregulated in patients with systemic inflammation and infection, but its functional role is unclear. We up- or downregulated UCP2 expression using UCP2 recombinant adenovirus or the UCP2 inhibitor, genipin, in lungs of mice, and investigated the mechanisms of UCP2 in ALI. UCP2 overexpression in mouse lungs increased LPS-induced pathological changes, lung permeability, lung inflammation, and lowered survival rates. Furthermore, ATP levels and mitochondrial membrane potential were decreased, while reactive oxygen species production was increased. Additionally, mit

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Wong, Aaron, Ricardo Zamel, Jonathan Yeung, Gary D. Bader, Claudia C. Dos Santos, Xiaohui Bai, Yubo Wang, Shaf Keshavjee, and Mingyao Liu. "Potential therapeutic targets for lung repair during human ex vivo lung perfusion." European Respiratory Journal 55, no. 4 (February 14, 2020): 1902222. http://dx.doi.org/10.1183/13993003.02222-2019.

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Abstract (sommario):

IntroductionThe ex vivo lung perfusion (EVLP) technique has been developed to assess the function of marginal donor lungs and has significantly increased donor lung utilisation. EVLP has also been explored as a platform for donor lung repair through injury-specific treatments such as antibiotics or fibrinolytics. We hypothesised that actively expressed pathways shared between transplantation and EVLP may reveal common mechanisms of injury and potential therapeutic targets for lung repair prior to transplantation.Materials and methodsRetrospective transcriptomics analyses were performed with pe

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Lopez, A., and R. Bildfell. "Pulmonary Inflammation Associated with Aspirated Meconium and Epithelial Cells in Calves." Veterinary Pathology 29, no. 2 (March 1992): 104–11. http://dx.doi.org/10.1177/030098589202900202.

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Abstract (sommario):

“Meconium aspiration syndrome” is a condition resulting in respiratory distress and the occasional death of newborn human beings. A retrospective study was conducted on 52 calves that were submitted for postmortem examination to the Atlantic Veterinary College, Charlottetown, Prince Edward Island, Canada. These calves died of infectious and noninfectious diseases within the first 2 weeks of life due to a variety of causes. The most common cause of death was infectious enteric disease. Histologic examination of lungs revealed that 42.5% of calves had evidence of meconium, squamous cells, or ker

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Yuan, Zhihong, Mansoor Syed, Dipti Panchal, Myungsoo Joo, Chetna Bedi, Sokbee Lim, Hayat Onyuksel, Israel Rubinstein, Marco Colonna, and Ruxana T. Sadikot. "TREM-1-accentuated lung injury via miR-155 is inhibited by LP17 nanomedicine." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 5 (March 1, 2016): L426—L438. http://dx.doi.org/10.1152/ajplung.00195.2015.

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Abstract (sommario):

Triggering receptors expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on myeloid cells. Synergy between TREM-1 and Toll-like receptor amplifies the inflammatory response; however, the mechanisms by which TREM-1 accentuates inflammation are not fully understood. In this study, we investigated the role of TREM-1 in a model of LPS-induced lung injury and neutrophilic inflammation. We show that TREM-1 is induced in lungs of mice with LPS-induced acute neutrophilic inflammation. TREM-1 knockout mice showed an improved survival after lethal doses of LPS with an attenu

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Nair, Meera. "The macrophage-derived proteins murine RELMα and human resistin regulate host immunity to helminth infection (MPF3P.801)". Journal of Immunology 192, № 1_Supplement (1 травня 2014): 132.1. http://dx.doi.org/10.4049/jimmunol.192.supp.132.1.

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Abstract (sommario):

Abstract Th2 cells are essential for protective immunity to helminths but also contribute to chronic inflammation. Here we identify the REsistin-Like Molecules RELMα and Resistin as critical mediators of this balance between helminth Th2-mediated immunity and inflammation in both murine infection and human studies. Following infection with Nippostrongylus brasiliensis, we observed significant macrophage expression of RELMα in the lungs. When RELMα-/- mice were infected with N. brasiliensis, there were increased Th2-type responses, accelerated worm expulsion and exacerbated lung inflammation co

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Kim, Tae Ho, Jun-Yong Choi, Kyun Ha Kim, Min Jung Kwun, Chang-Woo Han, Ran Won, Jung Ju Lee, Jong-In Kim, and Myungsoo Joo. "Hominis placenta Suppresses Acute Lung Inflammation by Activating Nrf2." American Journal of Chinese Medicine 46, no. 04 (January 2018): 801–17. http://dx.doi.org/10.1142/s0192415x18500428.

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Abstract (sommario):

Hominis placenta (HP), a dried human placenta, has been known to target liver, lung, or kidney meridians, improving the functions associated with these meridians in traditional Chinese or Asian medicine (TCM). Since recent studies implicate an HP extract in suppressing inflammation, we investigated whether an aqueous HP extract can ameliorate inflammation that occurred in the lungs. When administered with a single intratracheal lipopolysaccharide (LPS), C57BL/6 mice developed an acute neutrophilic lung inflammation along with an increased expression of pro-inflammatory cytokine genes. However,

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Preuss, Jonathan M., Ute Burret, Michael Gröger, Sandra Kress, Angelika Scheuerle, Peter Möller, Jan P. Tuckermann, Martin Wepler, and Sabine Vettorazzi. "Impaired Glucocorticoid Receptor Signaling Aggravates Lung Injury after Hemorrhagic Shock." Cells 11, no. 1 (December 30, 2021): 112. http://dx.doi.org/10.3390/cells11010112.

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Abstract (sommario):

We previously showed that attenuated lung injury after hemorrhagic shock (HS) coincided with enhanced levels of the glucocorticoid (GC) receptor (GR) in lung tissue of swine. Here, we investigated the effects of impaired GR signaling on the lung during resuscitated HS using a dysfunctional GR mouse model (GRdim/dim). In a mouse intensive care unit, HS led to impaired lung mechanics and aggravated lung inflammation in GRdim/dim mice compared to wildtype mice (GR+/+). After HS, high levels of the pro-inflammatory and pro-apoptotic transcription factor STAT1/pSTAT1 were found in lung samples from

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Lin, Hung-Jung, Chia-Ti Wang, Ko-Chi Niu, Chungjin Gao, Zhuo Li, Mao-Tsun Lin, and Ching-Ping Chang. "Hypobaric hypoxia preconditioning attenuates acute lung injury during high-altitude exposure in rats via up-regulating heat-shock protein 70." Clinical Science 121, no. 5 (May 20, 2011): 223–31. http://dx.doi.org/10.1042/cs20100596.

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Abstract (sommario):

HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the expression of HSP70 in lungs prior to the onset of HAE. At 2 weeks after the start of HHP, animals were exposed to a simulated HAE of 6000 m in a hypobaric chamber for 24 h. Immediately after being returned to ambient pressure, the non-HHP animals had higher scores of alveolar oedema, neutrophil infil

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Lagishetty, Venu, Prasanna Tamarapu Parthasarathy, Oluwakemi Phillips, Jutaro Fukumoto, Young Cho, Itsuko Fukumoto, Huynh Bao, et al. "Dysregulation of CLOCK gene expression in hyperoxia-induced lung injury." American Journal of Physiology-Cell Physiology 306, no. 11 (June 1, 2014): C999—C1007. http://dx.doi.org/10.1152/ajpcell.00064.2013.

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Abstract (sommario):

Hyperoxic acute lung injury (HALI) is characterized by inflammation and epithelial cell death. CLOCK genes are master regulators of circadian rhythm also implicated in inflammation and lung diseases. However, the relationship of CLOCK genes in hyperoxia-induced lung injury has not been studied. This study will determine if HALI alters CLOCK gene expression. To test this, wild-type and NALP3−/− mice were exposed to room air or hyperoxia for 24, 48, or 72 h. In addition, mice were exposed to different concentrations of hyperoxia (50, 75, or 100% O2) or room air for 72 h. The mRNA and protein lev

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