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Статті в журналах з теми "Lungs Inflammation":

1

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 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) (80 μg) in LSP1-deficient ( Lsp1−/−) and wild-type (WT) 129/SvJ mice. Immunocytochemistry and Western blots showed increased expression of LSP1 and phosphorylated LSP1 in lungs of LPS-treated WT mice. Histology showed more congestion, inflammation, and Gr-1+neutrophils in lung of WT mice than Lsp1−/−mice. LPS-treated WT mice had significantly more neutrophils in bronchoalveolar lavage (BAL) and myeloperoxidase levels in lungs compared with Lsp1−/−mice. However, there were no differences in lung tissue and BAL concentrations of keratinocyte-derived chemokine, monocyte chemoattractant protein-1, macrophage inflammatory protein-1α and -1β, vascular permeability, and phosphorylated p38 MAPK between LPS-treated WT and Lsp1−/−mice, whereas TNF-α concentration was higher in BAL fluid from LPS-treated WT. Immunoelectron microscopy showed increased LSP1 in the nuclei of LPS-treated neutrophils. We also found increased levels of phosphorylated LSP1 associated with plasma membrane, nucleus, and cytosol at various times after LPS treatment of murine bone marrow-derived neutrophils, suggesting its role in modulation of neutrophil cytoskeleton and the membrane. These data collectively show increased expression of LSP1 in inflamed mouse and human lungs and its role in neutrophil recruitment and lung inflammation.
2

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 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. Pharmacological inhibition of CatS resulted in a significant decrease in pulmonary inflammation, lung damage and mucus plugging in the lungs of βENaC-Tg mice. In addition, instillation of CatS into the lungs of WT mice resulted in inflammation, lung remodelling and upregulation of mucin expression. Inhibition of the CatS target, protease-activated receptor 2 (PAR2), in βENaC-Tg mice resulted in a reduction in airway inflammation and mucin expression, indicating a role for this receptor in CatS-induced lung pathology.Our data indicate an important role for CatS in the pathogenesis of CF-like lung disease mediated in part by PAR2 and highlight CatS as a therapeutic target.
3

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 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 weeks (obesity), and 26 weeks (morbid obesity). Overweight and morbidly obese mice were sensitized and challenged with ovalbumin (OVA) to induce allergic lung inflammation. The AdipoR1 expression was reduced significantly in the lung Helios+ and Helios− Tregs of obese mice compared with lean mice. Airway allergic inflammation showed reduced AdipoR1 expression in lung Foxp3+ Tregs. Obesity significantly exacerbated the eosinophilic airway inflammation and reduced the number of Helios+ Tregs in lung and adipose tissue in the obesity-associated asthma model. Upon further weight gain, AdipoR1-expressing Tregs in the lungs of allergic mice were increased, whereas AdipoR1-expressing Tregs in adipose tissue were reduced. These data suggest that obesity-associated adipose tissue inflammation may exacerbate allergic inflammation by downregulating the AdipoR1+ Tregs in the lungs.
4

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 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 lipopolysaccharide (LPS) 16 h earlier. SP-D clearance from lavage into lung tissue was time dependent from 5 min to 1 h and 1.7-fold greater in LPS-treated lungs than in control lungs. Analysis of cells isolated by enzymatic digestion of lung tissue revealed differences in the SP-D-positive cell population between groups. LPS-treated lungs had 28.1-fold more SP-D-positive tissue-associated neutrophils and 193.6-fold greater SP-D association with those neutrophils compared with control lungs. These data suggest that clearance of SP-D into lung tissue is increased during inflammation and that tissue-associated neutrophils significantly contribute to this process.
5

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 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 anterior, and lungs of mechanically ventilated healthy rats and in nonventilated control animals (n = 8/group) for 1 h, using two different strategies (moderate VT [VT = 9 ml/kg] and high VT [VT = 35 ml/kg]). Results The main findings are summarized as follows: compared with controls, (1) the diaphragms and gastrocnemius of high-VT rats exhibited a decrease in reactive carbonyls, (2) the soleus and tibialis of high- and moderate-VT rodents showed a reduction in reactive carbonyls and malondialdehyde-protein adducts, (3) the lungs of high-VT rats exhibited a significant rise in malondialdehyde-protein adducts, (4) the soleus and tibialis of both high- and moderate-VT rats showed a reduction in protein nitration, (5) the lungs of high- and moderate-VT rats showed a reduction in antioxidant enzyme levels, but not in the muscles, and (6) the diaphragms and gastrocnemius of all groups exhibited very low inflammatory cell counts, whereas the lungs of high-VT rats exhibited a significant increase in inflammatory infiltrates. Conclusions Although oxidative stress and inflammation increased in the lungs of rats exposed to high VT, the diaphragm and limb muscles exhibited a decline in oxidative stress markers and very low levels of cellular inflammation.
6

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 and the numbers of inflammatory infiltrates in bronchoalveolar lavage fluid (BALF) were characterized. The frequency, the number of Tregs, and the levels of Foxp3 expression in the lungs and IL-8, IL-35, and TNF-α in BALF were determined by flow cytometry, RT-PCR and ELISA, respectively. Treatment with erythromycin reduced smoking-induced inflammatory infiltrates, the levels of IL-8 and TNF-α in the BALF and lung damages but increased the numbers of CD4+Foxp3+Tregs and the levels of Foxp3 transcription in the lungs, accompanied by increased levels of IL-35 in the BALF of rats. Our novel data indicated that erythromycin enhanced Treg responses, associated with the inhibition of smoking-induced inflammation in the lungs of rats.
7

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 lung method to obtain and characterize lung perfusate from the pulmonary circulation. LPS administration to mouse lungs resulted in an increased release of inflammation-relevant cytokines and chemokines into the perfusate (Luminex assay) compared with the saline-controls. Subsequently, primary mouse liver vascular endothelial cells (LVEC) or mouse polymorphonuclear leukocytes (PMN) in vitro were stimulated with the perfusate obtained from saline- or LPS-challenged lungs and assessed for various inflammation-relevant end points. The obtained results indicate that stimulation of LVEC with perfusate obtained from LPS-challenged lungs results in 1) reactive oxygen species (ROS) production; 2) activation of NF-κB; and 3) expression of E-selectin, ICAM-1, and VCAM-1 and a subsequent increase in PMN rolling and adhesion to LVEC. In addition, perfusate from LPS-challenged lung induced activation of PMN with respect to increased ROS production and upregulation of cell surface levels of adhesion molecules MAC-1 and VLA-4. Heat-inactivation of the perfusate obtained from LPS-challenged lungs was very effective in suppressing increased proadhesive phenotype (i.e., E-selectin and ICAM-1 expression) in LVEC, whereas targeted inhibition (immunoneutralization) of TNF-α and/or IL-6 in LPS-lung perfusate had no effect. Taken together, these findings indicate that multiple proinflammatory mediators (proteinaceous in nature) released from inflamed lungs act synergistically to induce systemic activation of circulating PMN and promote inflammatory responses in liver vascular endothelial cells.
8

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 inflammation. Sheep underwent unilateral saline lung lavage and were ventilated supine for 4 h (positive end-expiratory pressure = 10 cmH2O, tidal volume adjusted to plateau pressure = 30 cmH2O). We used PET scans of injected 13N-nitrogen to compute regional perfusion and ventilation and injected 18F-FDG to calculate 18F-FDG uptake rate. Regional aeration was quantified with transmission scans. Whole lung 18F-FDG uptake was approximately two times higher in lavaged than in nonlavaged lungs (2.9 ± 0.6 vs. 1.5 ± 0.3 10−3/min; P < 0.05). The increased 18F-FDG uptake was topographically heterogeneous and highest in dependent low-aeration regions (gas fraction 10–50%, P < 0.001), even after correction for lung density and wet-to-dry lung ratios. 18F-FDG uptake in low-aeration regions of lavaged lungs was higher than that in low-aeration regions of nonlavaged lungs ( P < 0.05). This occurred despite lower perfusion and ventilation to dependent regions in lavaged than nonlavaged lungs ( P < 0.001). In contrast, 18F-FDG uptake in normally aerated regions was low and similar between lungs. Surfactant depletion produces increased and heterogeneously distributed pulmonary 18F-FDG uptake after 4 h of supine mechanical ventilation. Metabolic activity is highest in poorly aerated dependent regions, suggesting local increased inflammation.
9

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 bond between MMA and the toll-like receptor 4 (TLR- 4), namely, His 228, with a MolDock score of –43.677 kcal/mol. Microscopic examination of lungs confirmed that a greater number of inflammatory cells were found in the treatment group than in the control group and symptoms of inflammation were clearly observable after 120 min of exposure. Conclusion: Thus, inflammation occurring due to MMA interaction with TLR-4 receptors can be predicted in silico and exposure to 150 ppm MMA for more than 120 min can cause lung inflammation in mice.
10

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 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). Based on histological grading, lungs from dogs with ANP showed inflammation (median score, 1.5; range, 0–3), but the scores did not differ statistically from the control lungs (median score, 0.5; range, 0–2). A grid intersects-counting method showed an increase in the numbers of MAC387-positive alveolar septal mononuclear phagocyte profiles in lungs of dogs with ANP (ratio median, 0.0243; range, 0.0093–0.0734, with 2 outliers at 0.1523 and 0.1978) compared with controls (ratio median, 0.0019; range, 0.0017–0.0031; P < .0001). Only dogs with ANP showed labeling for von Willebrand factor in alveolar septal capillary endothelial cells, septal inflammatory cells, and alveolar macrophages. Toll-like receptor 4 and interleukin 6 were variably expressed in alveolar macrophages and septal inflammatory cells in lungs from both ANP and control dogs. Inducible nitric oxide synthase was detected in alveolar macrophages of dogs with ANP only. These data show that dogs with ANP have lung inflammation, including the recruitment of PIMs and expression of inflammatory mediators.

Дисертації з теми "Lungs Inflammation":

1

McLennan, Geoffrey. "Oxygen toxicity and radiation injury to the pulmonary system." Title page, index and forward only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phm164.pdf.

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Bibliography: leaves 168-184. The work in this study encompasses oxygen free radical related inflammation in the peripheral lung and in lung cells. Animal and human studies have been used. Methods include cell culture with function studies, protein chemistry, animal and human physiology, and cell and lung structure through histopathology, and various forms of electron microscopy. The work resulting from this thesis has formed an important basis for understanding acute and chronic lung injury.
2

Corsino, Betsy Ann 1962. "THE PULMONARY RESPONSE INDUCED BY GLASS FIBERS (INFLAMMATION, SILICOSIS, MURINE MODEL)." Thesis-Reproduction (electronic), The University of Arizona, 1986. http://hdl.handle.net/10150/291468.

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3

Dokka, Sujatha. "IL-10 gene therapy for the treatment of pulmonary inflammation." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1421.

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Thesis (Ph. D.)--West Virginia University, 2000.
Title from document title page. Document formatted into pages; contains ix, 132 p. : ill. (some col.) Vita. Includes abstract. Includes bibliographical references.
4

Finlay, Alison. "Kinetics of pulmonary eosinophilia in a mouse model." Electronic Thesis or Diss., University of York, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245971.

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5

Karandashova, Sophia. "The Role of Ceramide in Neutrophil Elastase Induced Inflammation in the Lungs." Text, VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5468.

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Alterations to sphingolipid metabolism are associated with increased pulmonary inflammation, but the impact of inflammatory mediators, such as neutrophil elastase (NE), on airway sphingolipid homeostasis remains unknown. NE is a protease associated CF lung disease progression, and can be found in up to micromolar concentrations in patient airways. While sphingolipids have been investigated in the context of CF, the focus has been on loss of cystic fibrosis transmembrane conductance regulator (CFTR) function. Here, we present a novel observation: oropharyngeal aspiration of NE increases airway ceramides in mice. Using a previously characterized mouse model of NE-induced inflammation, we demonstrate that NE increases de novo ceramide production, which is likely mediated via increased SPTLC2 levels. Inhibition of de novo sphingolipid synthesis using myriocin, an SPT inhibitor, decreases airway ceramide as well as the release of pro-inflammatory signaling molecules induced by NE. Furthermore, in a retrospective study of the sphingolipid content of CF sputum—the largest of its type in this patient cohort to date, we investigated the association between NE and sphingolipids. There were linear correlations between the concentration of active NE and ceramide, sphingomyelin, and monohexosylceramide moieties as well as sphingosine-1-phosphate. The presence of Methicillin-resistant Staphylococcus aureus (MRSA) positive culture and female gender both strengthened the association of NE and sphingolipids, but higher FEV1 % predicted weakened the association, and Pseudomonas aeruginosa had no effect on the association between NE and sphingolipids. These data suggest that NE may increase sphingolipids in CF airways as it did in our in vivo model, and that this association is stronger in patients that have worse lung function, are female, and whose lungs are colonized with MRSA. Modulating sphingolipid homeostasis could provide novel pharmacological approaches for alleviating pulmonary inflammation.
6

McDaniel, Dylan K. "Characterization of Biomedical and Incidental Nanoparticles in the Lungs and Their Effects on Health." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/86128.

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Nanomaterials are defined as any material with at least one external dimension less than 100 nm. Recently, nanomaterials have become more common in medicine, technology, and engineering. One reason for their increased interest is due to nanomaterials having unique properties that allow them to interact effectively with biological systems. In terms of drug delivery, the lungs are a highly desirable site to administer therapeutic nanoparticles. Indeed, inflammatory diseases such as asthma and emphysema could potentially benefit from nanoparticle-mediated delivery. However, the lungs are also in constant contact with airborne particulate matter. Thus, harmful nanoparticles can enter the lungs and cause or even exacerbate inflammatory diseases. Our work focused on characterization of both therapeutic and potentially harmful nanoparticles in the lungs. We found that fluorescently-labeled nanoparticles were phagocytosed by macrophages and did not induce apoptosis or inflammation in the lungs, making them potentially useful as a therapeutic for inflammatory diseases. We also characterized a rare form of titanium-based particles called Magnéli phases, which have been shown to be produced via coal burning. We found that while these particles are non-inflammatory in the lungs of mice, they lead to apoptosis of macrophages as well as a change in gene expression associated with increased fibrosis. Ultimately, this was shown to lead to a decrease in lung function parameters and airway hyperresponsiveness, indicating increased lung stiffness after long-term nanoparticle exposure. Our data adds significant contributions to the field by assessing two nanoparticles with vastly different compositions in the lungs. Overall, we found that the unique properties of both particle types allows for interactions with cells and tissues. These interactions can have important outcomes on health, both in terms of disease treatment and exacerbation.
Ph. D.
Over the years, nanoparticles have become more common in medicine, technology, and engineering due to their unique properties. Many of these properties allow for increased interactions with biological materials. Organs such as the lungs are at increased risk of exposure because they naturally encounter microorganisms and airborne particles on a daily basis. However, the lungs are also a highly desirable site for drug delivery using nanoparticles, due to ease of access. Inflammatory diseases such as asthma and emphysema could potentially benefit from nanoparticle-mediated delivery. Additionally, harmful nanoparticles can enter the lungs and cause or even exacerbate these diseases. Unfortunately, there is a lack of knowledge pertaining to this subject. Our work focused on assessing the interactions of nanoparticles in the lungs. First, we looked at nanoparticles that could be used for drug delivery. We found that fluorescentlylabeled nanoparticles were taken up by phagocytic white blood cells called macrophages. Furthermore, these particles did not induce cell death or inflammation in the lungs. Therefore, we found that these particles could be useful for drug delivery in the lungs. Secondly, we investigated potentially harmful nanoparticles and their effects on the lungs. The titanium-based particles called Magnéli phases, have been shown to be produced through coal burning. We found that while these particles are non-inflammatory in the lungs, they do lead to programmed death of macrophages as well as the increase in genes associated with fibrosis. Ultimately these particles led to a decrease in lung function after long-term exposure.
7

Zheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.

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8

Lewis, Joshua B. "Alterations in Tight Junctional Proteins and Their Effects on Pulmonary Inflammation." Text, BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6308.

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The lungs represent one of the earliest interfaces for pathogens and noxious stimuli to interact with the body. As such, careful maintenance of the permeability barrier is vital in providing homeostasis within the lung. Essential to maintaining this barrier is the tight junction, which primarily acts as a paracellular seal and regulator of ionic transport, but also contributes to establishing cell polarity, cell-to-cell integrity, and regulating cell proliferation and differentiation. The loss of these tight junctions has been documented to result in alterations in inflammation, and ultimately the development of many respiratory disorders such as COPD, Asthma, ARDS, and pulmonary fibrosis. One critical contributor that creates this permeability barrier is the tight junctional protein Claudin. While studies have begun to elucidate the various functions and roles of various Claudins, our understanding is still limited. To initially investigate these proteins, we looked at both temporal and spatial expression patterns for family members during development. A consistent pattern was demonstrated in mRNA expression for the majority of Claudin members. In general, Claudin expression underwent rapid increase during time periods that correlate with the pseudoglanduar/canalicular periods. One notable exception was Claudin 6 (Cldn6), which demonstrated decreasing levels of mRNA expression throughout gestation. We also sought to understand expression dynamics during the addition of maternal secondhand smoke (SHS) which resulted in an almost universal decrease in Claudin proteins. To more fully explore expression mechanisms that affect Claudin-6 (Cldn6), we exposed pulmonary alveolar type II (A549) cells to cigarette smoke extract (CSE) and found that it transcriptionally regulated Cldn6 expression. Using a luciferase reporter, we determined that transcription was negatively regulated at multiple promoter response elements by CSE, and transcription was equally hindered by hypoxic conditions. These findings identified Cldn6 as a potential target of SHS and other respiratory irritants such as diesel particulate matter (DPM). We next sought to assess whether an increase in Cldn6 was sufficient to provide a protective advantage against harmful exogenous exposure. To test this, we utilized a doxycycline induced Cldn6 over-expressing mouse, and subjected it to SHS for 30 days to stimulate an inflammatory state. Our findings demonstrated that Cldn6 transgenic animals have decreased inflammation as evidence by decreased total cell infiltration into the airways, decreased polymorphonuclocyte (PMNs) extravasation, total protein in bronchoalveolar lavage fluid (BALF), and decreased cytokine secretion. Anti-inflammatory advantages were also discovered during experiments involving acute exposure to DPM. In both cases, while stimulation of transgenic mice with SHS or DPM diminished Cldn6 expression, anti-inflammatory evidence emerged suggesting that genetic up-regulation of Cldn6 likely causes the recruitment of other tight junctional components during an organism's response to environmental assault.
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Lau, Kwok-wai, and 劉國威. "The involvement of serotoninergic system in cigarette smoke-induced oxidative stress and inflammation: relevantto chronic obstructive pulmonary disease." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47869616.

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Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD) with chronic airway inflammation as a key feature. Currently, no effective treatment can reduce the protracted inflammation in the lung of COPD. Further research on the inflammatory mechanisms would therefore be important in determining new potential therapeutic targets in COPD. Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter that plays an important role in pulmonary functions and inflammatory responses. The serotoninergic system including serotonin transporter (SERT), serotonin receptors (5-HTR) and its metabolic enzyme monoamine oxidase (MAO) have been reported to associate with cigarette smoking and/or COPD. Blockade of serotonin receptor 2A (5-HTR2A) with its selective antagonist ketanserin has been shown to improve lung function in COPD patients. In this study, we hypothesize that the serotoninergic system is involved in cigarette smoke-induced oxidative stress, inflammation and COPD. Exposure to cigarette smoke medium (CSM) caused the elevation of interleukin (IL)-8 levels in primary normal human bronchial epithelial (NHBE) cells and a human bronchial epithelial cell line (BEAS-2B) in vitro via activation of p38 and extracellular signal-regulated kinases 1 and 2 (ERK1/2) signaling pathway. Besides, CSM was found to disrupt the glutathione (GSH) system, resulting in the translocation of nuclear factor-erythroid 2 related factor 2 (Nrf2) to the nucleus. Knock-down of Nrf2 by small interference RNA (siRNA) blocked CSM-induced IL-8 release. Pretreatment with ketanserin was found to attenuate CSM-induced IL-8 release by inhibiting the p38, ERK1/2, and Nrf2 signaling pathways, and by partially restoring the GSH system. On the other hand, CSM reduced MAO activity in BEAS-2B, indicating a reduced catabolism of 5-HT. Furthermore, 5-HT was found to share the common p38 and ERK1/2 signaling pathway with CSM in IL-8 release. In the cigarette smoke-exposed rat model, the GSH system in the lung was found to be disrupted compared to the sham-air control, supporting our in vitro findings. Interestingly, we found an increased MAO-A activity in the lung of cigarette smoke-exposed rats in comparison to sham air-exposed rats. The increased MAO-A activity in the lung was associated with the reduction of 5-HT levels in bronchoalveolar lavage (BAL) and lung homogenates, while the increased metabolism of 5-HT may be involved in cigarette smoke-induced superoxide anion levels. On the other hand, serum, but not plasma level of 5-HT was elevated in cigarette smoke-exposed group, which may be due to platelet activation caused by cigarette smoke. In the clinical study, the elevated plasma 5-HT levels were found to be associated with an increased odds ratio for COPD and positively correlated with age in COPD patients. Furthermore, plasma 5-HT was also demonstrated to be a significant mediator on the relation between cigarette smoking and COPD. In summary, our study supports the hypothesis that the serotoninergic system contributes to cigarette smoke-induced oxidative stress, inflammation and COPD. The serotoninergic system (e.g. 5-HTR2A) may constitute potential therapeutic targets for the treatment of COPD, which is worthy for further investigation.
published_or_final_version
Medicine
Doctoral
Doctor of Philosophy
10

McNamara, Tracy Renee. "Chlamydia pneumoniae and airways inflammation : an investigation of the host cell-pathogen relationship /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phm4791.pdf.

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Книги з теми "Lungs Inflammation":

1

Symposium, on Airway Obstruction and Inflammation (1988 Florence Italy). Airway obstruction and inflammation: Present status and perspectives. Basel: Karger, 1990.

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2

Bertolini, Renzo. Animal and vegetable dusts as a cause of deep lung inflammation. Hamilton: CCOHS, 1988.

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3

Rogers, Thomas J., Gerard J. Criner, and William D. Cornwell, eds. Smoking and Lung Inflammation. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0.

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4

Dubinett, Steven M., ed. Inflammation and Lung Cancer. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1.

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5

Alper, Scott, and William J. Janssen, eds. Lung Innate Immunity and Inflammation. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8.

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6

Wang, Yong-Xiao, ed. Lung Inflammation in Health and Disease, Volume I. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63046-1.

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7

Wang, Yong-Xiao, ed. Lung Inflammation in Health and Disease, Volume II. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68748-9.

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8

Criner, Gerard J., William D. Cornwell, and Thomas J. Rogers. Smoking and lung inflammation: Basic, pre-clinical, and clinical research advances. New York: Springer, 2013.

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9

Cells and cytokines in lung inflammation. New York, NY: New York Academy of Sciences, 1994.

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10

Cytokines and adhesion molecules in lung inflammation. New York: New York Academy of Sciences, 1996.

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Частини книг з теми "Lungs Inflammation":

1

Marleau, S., C. Fortin, and P. Borgeat. "In Vivo Desensitization to LTB4-Induced Neutrophil Sequestration in Rabbit Lungs." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 261–63. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_51.

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2

Ulges, Alexander, Edgar Schmitt, Tobias Bopp, and Matthias Klein. "Messenger RNA Sequencing of Rare Cell Populations in the Lung and Lung-Draining Lymph Nodes." In Inflammation, 199–219. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6786-5_14.

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3

Sharma, Sherven, Siwen Hu-Lieskovan, Steven M. Dubinett, and Jay Moon Lee. "Inflammation and Lung Cancer: Addressing Inflammation with Immunotherapy." In Inflammation and Lung Cancer, 191–209. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_7.

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4

Kennedy, Paul A., and Laurie E. Kilpatrick. "Neutrophil Inflammation in COPD." In Smoking and Lung Inflammation, 59–79. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_3.

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5

Taraseviciene-Stewart, Laimute, and Norbert F. Voelkel. "Immunopathology of COPD." In Smoking and Lung Inflammation, 1–27. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_1.

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6

Barnes, Peter J. "Anti-Inflammatory Therapeutics in COPD: Past, Present, and Future." In Smoking and Lung Inflammation, 191–213. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_10.

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7

Cornwell, William D., Maria Elena Vega, and Thomas J. Rogers. "Monocyte Populations Which Participate in Chronic Lung Inflammation." In Smoking and Lung Inflammation, 29–58. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_2.

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8

Kim, Victor, Kosuke Kato, K. Chul Kim, and Erik P. Lillehoj. "Role of Epithelial Cells in Chronic Inflammatory Lung Disease." In Smoking and Lung Inflammation, 81–98. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_4.

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9

Song, Changcheng, and Steven G. Kelsen. "The Relationship Between Oxidative Stress Responses and Lung Inflammation with Cigarette Smoking." In Smoking and Lung Inflammation, 99–127. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_5.

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10

Corry, David B., and Farrah Kheradmand. "Autoimmune Mechanisms Contributing to Chronic Obstructive Pulmonary Disease." In Smoking and Lung Inflammation, 129–42. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_6.

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Тези доповідей конференцій з теми "Lungs Inflammation":

1

Torres-Gonzalez, Edilson, Jeffrey D. Ritzenthaler, and Jesse Roman-Rodriguez. "Modulation Of Inflammation By Mid-Cervical Vagotomy In Murine Lungs." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5131.

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2

Kuroda, E., and KJ Ishii. "1707c Inhaled fine particles induce allergic inflammation in the lungs." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.145.

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3

Wall, Wolfgang A., Andrew Comerford, Lena Wiechert, and Sophie Rausch. "Coupled and Multi-Scale Building Blocks for a Comprehensive Computational Lung Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206407.

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Анотація:
Mechanical ventilation is a vital supportive therapy for critical care patients suffering from Acute Respiratory Distress syndrome (ARDS) or Acute Lung Injury (ALI) in view of oxygen supply. However, a number of associated complications often occur, which are collectively termed ventilator induced lung injuries (VILI) [1]. Biologically, these diseases manifest themselves at the alveolar level and are characterized by inflammation of the lung parenchyma following local overdistension or high shear stresses induced by frequent alveolar recruitment and derecruitment. Despite the more recent adoption of protective ventilation strategies based on the application of lower tidal volumes and a positive end-expiratory pressure (PEEP), patient mortality rates are with approximately 40% still very high. Understanding the reason why the lungs still become damaged or inflamed during mechanical ventilation is a key question sought by the medical community. In this contribution, an overview on recently developed building blocks of a comprehensive lung model will be given, with a main focus on lower airways.
4

Shirai, Atsushi, and Toshiyuki Hayase. "Effect of Neutrophils Retention Time in Capillaries on Increase in Their Concentration in a Lattice Capillary Network Model." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176717.

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Neutrophils are known as the most popular cells in leukocytes, and play important roles in immune system. They are retained in pulmonary capillary network even in normal lungs, causing higher concentration than in systemic circulation due to their low deformability [1]. The lungs can be a route for pathogenic substances to invade the host, since thickness of septa which separates blood and outer air is extremely thin. However, the highly concentrated neutrophils are thought to be effectively recruited to the sites of inflammation for the host defense. Therefore, it is essential to know how neutrophils flow in pulmonary capillary microvasculature for the understanding of their functions and behavior in immune system.
5

Glasser, Stephan W., Melissa D. Maxfield, Teah L. Witt, John E. Baatz, Henry T. Akinbi, and Tom Korfhagen. "LPS Exposure Increases Inflammation In The Lungs Of SP-C Deficient Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2454.

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6

Zhou, Haiying, Shawn He, Sean Gunsten, Steven Brody, Walter Akers, and Mikhail Y. Berezin. "NIR fluorescent contrast agents for detection of inflammation of lungs in vivo." In CLEO: Applications and Technology. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/cleo_at.2014.am2p.1.

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7

Odom, C., Y. Kim, F. T. Korkmaz, E. Na, L. Baird, M. R. Jones, J. P. Mizgerd, K. Traber, and L. J. Quinton. "Liver Activity Reprograms the Lungs During Systemic Inflammation to Fortify Pulmonary Defense." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1262.

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8

Chan, Y. L., B. Wang, H. Chen, K. F. Ho, and B. Oliver. "Impact of Traffic Related Air Pollutant Exposure on Lung Inflammation and Mitochondrial Wellbeing in Mouse Lungs." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1832.

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9

Titova, Olga, Natalya Kuzubova, Elena Lebedeva, Tatiana Preobrajenskaya, and Elizaveta Volchkova. "Influence of induced immunosupression on inflammation and lungs remodeling on the COPD model." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3853.

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10

Hamburg, Brian, Mei Hulver, Zeyu Xiong, Jeffrey Isenberg, and Janet S. Lee. "A Lack Of Thrombospondin-1 Predisposes The Lungs To Inflammation Following Exposure To Endotoxin." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1087.

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Звіти організацій з теми "Lungs Inflammation":

1

Burgess, Jefferey L. Acute Lung Injury Following Smoke Inhalation: Predictive Value of Sputum Biomarkers and Time Course of Lung Inflammation. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada446886.

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2

Burgess, Jefferey L. Acute Lung Injury Following Smoke Inhalation: Predictive Value of Sputum Biomarkers and Time Course of Lung Inflammation. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada424038.

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3

Burgess, Jefferey L. Acute Lung Injury Following Smoke Inhalation: Predictive Value of Sputum Biomarkers and Time Course of Lung Inflammation. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada472079.

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