Journal articles: 'Pulmonary acute inflammation'

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Arndt, Patrick G., Brian Strahan, Yue Wang, Chunmei Long, Keisuke Horiuchi, and Bruce Walcheck. "Leukocyte ADAM17 Regulates Acute Pulmonary Inflammation." PLoS ONE 6, no. 5 (May 16, 2011): e19938. http://dx.doi.org/10.1371/journal.pone.0019938.

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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 underlying the transition from acute lung inflammation to pulmonary fibrosis, and the search for new molecular markers and promising therapeutic targets to prevent pulmonary fibrosis development, remain highly relevant tasks. This review focuses on the etiology, pathogenesis, morphological characteristics and outcomes of acute lung inflammation as a precursor of pulmonary fibrosis; the pathomorphological changes in the lungs during fibrosis development; the known molecular mechanisms and key players of the signaling pathways mediating acute lung inflammation and pulmonary fibrosis, as well as the characteristics of the most common in vivo models of these processes. Moreover, the prognostic markers of acute lung injury severity and pulmonary fibrosis development as well as approved and potential therapeutic approaches suppressing the transition from acute lung inflammation to fibrosis are discussed.

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Eckle, Tobias, Michael Koeppen, and Holger K. Eltzschig. "Role of Extracellular Adenosine in Acute Lung Injury." Physiology 24, no. 5 (October 2009): 298–306. http://dx.doi.org/10.1152/physiol.00022.2009.

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Acute lung injury (ALI) is a lung disease characterized by pulmonary edema and severe hypoxia. The past decade hosted a search for endogenous mechanisms controlling lung inflammation and pulmonary edema during ALI. As such, recent evidence indicates extracellular adenosine in orchestrating the resolution of pulmonary edema and inflammation during ALI.

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Spond, J., N. Case, R. W. Chapman, Y. Crawley, R. W. Egan, J. Fine, J. A. Hey, et al. "Inhibition of experimental acute pulmonary inflammation by pirfenidone." Pulmonary Pharmacology & Therapeutics 16, no. 4 (August 2003): 207–14. http://dx.doi.org/10.1016/s1094-5539(03)00026-9.

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Singh, Baljit, Jacqueline W. Pearce, Lakshman N. Gamage, Kyathanahalli Janardhan, and Sarah Caldwell. "Depletion of pulmonary intravascular macrophages inhibits acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 2 (February 2004): L363—L372. http://dx.doi.org/10.1152/ajplung.00003.2003.

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Pulmonary intravascular macrophages (PIMs) are present in ruminants and horses. These species are highly sensitive to acute lung inflammation compared with non-PIM-containing species such as rats and humans. There is evidence that rats and humans may also recruit PIMs under certain conditions. We investigated precise contributions of PIMs to acute lung inflammation in a calf model. First, PIMs were recognized with a combination of in vivo phagocytic tracer Monastral blue and postembedding immunohistology with anti-CD68 monoclonal antibody. Second, gadolinium chloride depleted PIMs within 48 h of treatment ( P < 0.05). Finally, PIMs contain TNF-α, and their depletion reduces cells positive for IL-8 ( P < 0.05) and TNF-α ( P < 0.05) and histopathological signs of acute lung inflammation in calves infected with Mannheimia hemolytica. The majority of IL-8-positive inflammatory cells in lung septa of infected calves were platelets. Platelets from normal cattle contained preformed IL-8 that was released upon in vitro exposure to thrombin ( P < 0.05). These novel data show that PIMs, as the source of TNF-α, promote recruitment of inflammatory cells including IL-8-containing platelets to stimulate acute inflammation and pathology in lungs. These data may also be relevant to humans due to our ability to recruit PIMs.

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Selby, C., and W. Macnee. "Factors Affecting Neutrophil Transit During Acute Pulmonary Inflammation: Minireview." Experimental Lung Research 19, no. 4 (January 1993): 407–28. http://dx.doi.org/10.3109/01902149309064355.

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Mirakaj, Valbona, Cyril A. Thix, Stefanie Laucher, Carina Mielke, Julio C. Morote-Garcia, Marthe A. Schmit, Janek Henes, Klaus E. Unertl, David Köhler, and Peter Rosenberger. "Netrin-1 Dampens Pulmonary Inflammation during Acute Lung Injury." American Journal of Respiratory and Critical Care Medicine 181, no. 8 (April 15, 2010): 815–24. http://dx.doi.org/10.1164/rccm.200905-0717oc.

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Mancuso, Peter. "Obesity and lung inflammation." Journal of Applied Physiology 108, no. 3 (March 2010): 722–28. http://dx.doi.org/10.1152/japplphysiol.00781.2009.

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The prevalence of obesity has increased dramatically worldwide, predisposing individuals to an increased risk of morbidity and mortality due to cardiovascular disease and type 2 diabetes. Less recognized is the fact that obesity may play a significant role in the pathogenesis of pulmonary diseases through mechanisms that may involve proinflammatory mediators produced in adipose tissue that contribute to a low-grade state of systemic inflammation. In animal models, inflammatory responses in the lung have been shown to influence the production of the adipocytokines, leptin and adiponectin, cytokines, acute phase proteins, and other mediators produced by adipose tissue that may participate in immune responses of the lung. An increased adipose tissue mass may also influence susceptibility to pulmonary infections, enhance pulmonary inflammation associated with environmental exposures, and exacerbate airway obstruction in preexisting lung disease. An increased understanding of the mechanisms by which obesity influences pulmonary inflammation may facilitate the development of novel therapeutic interventions for the treatment of lung disease.

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Jung, Ayoung, Sung-Hyun Kim, Jun-Young Yang, Jayoung Jeong, Jong Kwon Lee, Jae-Ho Oh, and Jin Hee Lee. "Effect of Pulmonary Inflammation by Surface Functionalization of Zinc Oxide Nanoparticles." Toxics 9, no. 12 (December 6, 2021): 336. http://dx.doi.org/10.3390/toxics9120336.

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Zinc oxide nanoparticles (ZnO NPs) are used in various industries such as food additives, cosmetics, and biomedical applications. In this study, we evaluated lung damage over time by three types of ZnO NPs (L-serine, citrate, and pristine) following the regulation of functional groups after a single intratracheal instillation to rats. The three types of ZnO NPs showed an acute inflammatory reaction with increased LDH and inflammatory cell infiltration in the alveoli 24 h after administration. Especially in treatment with L-serine, citrate ZnO NPs showed higher acute granulocytic inflammation and total protein induction than the pristine ZnO NPs at 24 h. The acute inflammatory reaction of the lungs recovered on day 30 with bronchoalveolar fibrosis. The concentrations of IL-4, 6, TNF-α, and eotaxin in the bronchoalveolar lavage fluid (BALF) decreased over time, and the levels of these inflammation indicators are consistent with the following inflammatory cell data and acute lung inflammation by ZnO NP. This study suggests that single inhalation exposure to functionalized ZnO NPs may cause acute lung injury with granulocytic inflammation. Although it can recover 30 days after exposure, acute pulmonary inflammation in surface functionalization means that additional studies of exposure limits are needed to protect the workers that produce it.

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Ziablitsev, D. S., O. O. Dyadyk, and S. V. Ziablitsev. "ACTIVITY OF ANGIOTENSIN-CONVERSING ENZYME-2 IN ACUTE PULMONARY INFLAMMATION." Medical Science of Ukraine (MSU) 17, no. 3 (September 30, 2021): 3–14. http://dx.doi.org/10.32345/2664-4738.3.2021.01.

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Relevance. Angiotensin converting enzyme-2 (ACE2), which is the gateway to coronavirus, is also an important component of the tissue renin-angiotensin system with a number of anti-inflammatory effects. It is known that ACE2 is expressed in the lungs of patients with coronavirus pneumonia, but it is not clear how this depends on the stages of development and the severity of inflammation. Objective: to establish the effect of acute inflammation on pulmonary expression of angiotensin-converting enzyme-2. Material and methods. In Wistar rats (n=20), in compliance with bioethical standards, a sterile nylon thread 2.5 cm long and 0.2 mm thick to a depth of 2.5 cm was introduced into the trachea. The animals were observed and removed from the experiment at 7, 14, 21 and 28 days, microscopic and immunohistochemical (monoclonal antibodies against ACE2; clone 4G5.1; EMD Millipore Corporation; Temecula, CA US) studies were performed. Results. The microscopic picture of the lungs indicated the development of acute bronchopulmonary inflammation during the first week, the formation of peribronchial and alveolar abscesses in the second week with the onset of resolution of bronchopneumonia with the organization of abscesses in the third week and the development of diffuse fibrosis of the parenchyma and vascular hyalinosis in the fourth week of observation. The exudative phase of acute inflammation was accompanied by inhibition of ACE2 activity in bronchial epithelial cells, type II alveolocytes and vascular endothelium. With the transition of inflammation to the stage of proliferation and fibrosis, ACE2 activity was restored. Conclusion. The detected phase change in ACE2 activity can cause a wavy recurrent course of coronavirus infection, since an increase in the amount of ACE2 protein during attenuation of acute inflammation contributes to an increase in target cell infection.

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Xie, Yifang, Dehui Xie, Bin Li, and Hang Zhao. "Gender Differences in Low-Molecular-Mass-Induced Acute Lung Inflammation in Mice." International Journal of Molecular Sciences 22, no. 1 (January 3, 2021): 419. http://dx.doi.org/10.3390/ijms22010419.

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Gender differences in pulmonary inflammation have been well documented. Although low molecular mass hyaluronan (LMMHA) is known to trigger pulmonary lung inflammation, sex differences in susceptibility to LMMHA are still unknown. In this study, we test the hypothesis that mice may display sex-specific differences after LMMHA administration. After LMMHA administration, male mice have higher neutrophil, cytokine, and chemokine counts compared to that of their female counterparts. Additionally, Ovariectomized (OVX) mice show greater LMMHA-induced inflammation compared to that of mice with intact ovaries. Injections of OVX mice with 17β-estradiol can decrease inflammatory responses in the OVX mice. These results show that ovarian hormones regulate LMMHA induced lung inflammation.

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Wang, Yanbo, Hongwei Liang, Fangfang Jin, Xin Yan, Guifang Xu, Huanhuan Hu, Gaoli Liang, et al. "Injured liver-released miRNA-122 elicits acute pulmonary inflammation via activating alveolar macrophage TLR7 signaling pathway." Proceedings of the National Academy of Sciences 116, no. 13 (March 13, 2019): 6162–71. http://dx.doi.org/10.1073/pnas.1814139116.

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Hepatic injury is often accompanied by pulmonary inflammation and tissue damage, but the underlying mechanism is not fully elucidated. Here we identify hepatic miR-122 as a mediator of pulmonary inflammation induced by various liver injuries. Analyses of acute and chronic liver injury mouse models confirm that liver dysfunction can cause pulmonary inflammation and tissue damage. Injured livers release large amounts of miR-122 in an exosome-independent manner into the circulation compared with normal livers. Circulating miR-122 is then preferentially transported to mouse lungs and taken up by alveolar macrophages, in which it binds Toll-like receptor 7 (TLR7) and activates inflammatory responses. Depleting miR-122 in mouse liver or plasma largely abolishes liver injury-induced pulmonary inflammation and tissue damage. Furthermore, alveolar macrophage activation by miR-122 is blocked by mutating the TLR7-binding GU-rich sequence on miR-122 or knocking out macrophage TLR7. Our findings reveal a causative role of hepatic miR-122 in liver injury-induced pulmonary dysfunction.

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Kwak, Ho Geun, and Heung-Bin Lim. "Ligustrum lucidum Fruits Extract Inhibits Acute Pulmonary Inflammation in Mice." Korean Journal of Medicinal Crop Science 21, no. 5 (October 30, 2013): 323–28. http://dx.doi.org/10.7783/kjmcs.2013.21.5.323.

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Huang, Wen-Chung, Shu-Ju Wu, Ya-Ling Chen, Chwan-Fwu Lin, and Chian-Jiun Liou. "Tomatidine Improves Pulmonary Inflammation in Mice with Acute Lung Injury." Mediators of Inflammation 2021 (September 7, 2021): 1–11. http://dx.doi.org/10.1155/2021/4544294.

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Tomatidine, which is isolated from green tomato, can ameliorate inflammation and oxidative stress in cells and animal experiments and has been shown to improve airway inflammation in a murine model of asthma. Here, we investigated whether tomatidine can ameliorate acute lung injury in mice. Mice were given tomatidine by intraperitoneal injection for 7 consecutive days, and then, lung injury was induced via intratracheal instillation of lipopolysaccharide (LPS). Tomatidine reduced inflammatory cytokine expressions in bronchoalveolar lavage fluid (BALF), attenuated neutrophil infiltration in the BALF and lung tissue, increased superoxide dismutase activity and glutathione levels, and alleviated myeloperoxidase expression in the lung tissue of mice with lung injury. Tomatidine also decreased inflammatory cytokine and chemokine gene expression in inflammatory lungs and attenuated the phosphorylation of mitogen-activated protein kinase and nuclear factor kappa B. Furthermore, tomatidine enhanced the production of heme oxygenase-1, decreased the secretion of inflammatory cytokines and chemokines in LPS-stimulated lung epithelial cells, and attenuated THP-1 monocyte adhesion. Our findings suggest that tomatidine attenuates oxidative stress and inflammation, improving acute lung injury in mice.

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Blake, Terri L., and Mark J. Reasor. "Acute pulmonary inflammation in hamsters following intratracheal administration of amiodarone." Inflammation 19, no. 1 (February 1995): 55–65. http://dx.doi.org/10.1007/bf01534380.

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Deaton, Christopher M., David J. Marlin, Nicola C. Smith, Patricia A. Harris, Mark P. Dagleish, Robert C. Schroter, and Frank J. Kelly. "EFFECT OF ACUTE AIRWAY INFLAMMATION ON THE PULMONARY ANTIOXIDANT STATUS." Experimental Lung Research 31, no. 7 (January 2005): 653–70. http://dx.doi.org/10.1080/01902140591007092.

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Geraets, Liesbeth, Astrid Haegens, Antje R. Weseler, Karen Brauers, Juanita H. J. Vernooy, Emiel F. M. Wouters, Aalt Bast, and Geja J. Hageman. "Inhibition of acute pulmonary and systemic inflammation by 1,7-dimethylxanthine." European Journal of Pharmacology 629, no. 1-3 (March 2010): 132–39. http://dx.doi.org/10.1016/j.ejphar.2009.11.064.

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Zhao, Chunzhen, Jianbo Sun, Chunyan Fang, and Fadi Tang. "1,8-Cineol Attenuates LPS-Induced Acute Pulmonary Inflammation in Mice." Inflammation 37, no. 2 (November 8, 2013): 566–72. http://dx.doi.org/10.1007/s10753-013-9770-4.

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Yang, Yue, Yanan Cao, Gang Qin, Lu Wang, Qian Li, Sisi Dai, Lizhe Guo, et al. "Long non-coding RNA expression profiling in the lungs of pulmonary arterial hypertension rats with acute inflammation." Pulmonary Circulation 9, no. 4 (October 2019): 204589401987939. http://dx.doi.org/10.1177/2045894019879393.

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Background We performed RNA-sequencing to investigate the changes and expression profiles in long non-coding RNAs (lncRNAs) and their potential functional roles in the lungs of pulmonary arterial hypertension rats responding to acute inflammation. Methods To establish a pulmonary arterial hypertension rat model, monocrotaline was injected intraperitoneally and lipopolysaccharide was given to induce acute inflammation. Selected lncRNAs were validated by quantitative real-time polymerase chain reaction (qRT-PCR). Bioinformatics analyses were carried out to predict the potential biological roles of key lncRNAs. Results Twenty-eight lncRNAs and seven mRNAs with elevated expression and 202 lncRNAs and 36 mRNAs with decreased expression were found in the lung tissues of lipopolysaccharide-treated pulmonary arterial hypertension rats compared with control group. The qRT-PCR validation results were consistent with the bioinformatics analysis. Gene ontology analyses showed that the mRNAs and lncRNAs were differentially expressed in different pathways regarding biological process, cellular components, and molecular function. The functions of differentially expressed messenger RNAs (DEmRNAs) and DElncRNAs were indicated by Kyoto Encyclopedia of Genes and Genomes enrichment. Conclusion The DEmRNAs co-expressed with DElncRNAs were obviously enriched in inflammation. DElncRNAs and DEmRNAs in the lungs of pulmonary arterial hypertension rats changed with acute inflammation may provide new insights into the pathogenesis of pulmonary arterial hypertension.

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Baker, Emma H., David M. Wood, Amanda L. Brennan, Nicholas Clark, Deborah L. Baines, and Barbara J. Philips. "Hyperglycaemia and pulmonary infection." Proceedings of the Nutrition Society 65, no. 3 (August 2006): 227–35. http://dx.doi.org/10.1079/pns2006499.

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Pathophysiological stress from acute illness causes metabolic disturbance, including altered hepatic glucose metabolism, increased peripheral insulin resistance and hyperglycaemia. Acute hyperglycaemia is associated with increased morbidity and mortality in patients in intensive care units and patients with acute respiratory disease. The present review will consider mechanisms underlying this association. In normal lungs the glucose concentration of airway secretions is approximately 10-fold lower than that of plasma. Low airway glucose concentrations are maintained against a concentration gradient by active glucose transport. Airway glucose concentrations become elevated if normal homeostasis is disrupted by a rise in blood glucose concentrations or inflammation of the airway epithelium. Elevated airway glucose concentrations are associated with and precede increased isolation of respiratory pathogens, particularly methicillin-resistantStaphylococcus aureus, from bronchial aspirates of patients intubated on intensive care. Markers of elevated airway glucose are associated with similar patterns of respiratory infection in patients admitted with acute exacerbations of chronic obstructive pulmonary disease. Glucose at airway concentrations stimulates the growth of respiratory pathogens, over and above the effect of other nutrients. Elevated airway glucose concentrations may also worsen respiratory disease by promoting local inflammation. Hyperglycaemia may thus promote pulmonary infection, at least in part, by an effect on airway glucose concentrations. Therapeutic options, including systemic control of blood glucose and local manipulation of airway glucose homeostasis, will be considered.

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Hubeau, Cedric, John E. Kubera, Katherine Masek-Hammerman, and Cara M. M. Williams. "Interleukin-6 neutralization alleviates pulmonary inflammation in mice exposed to cigarette smoke and poly(I:C)." Clinical Science 125, no. 10 (July 16, 2013): 483–93. http://dx.doi.org/10.1042/cs20130110.

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Increased systemic and pulmonary levels of IL-6 (interleukin-6) are associated with the severity of exacerbations and decline of lung function in patients with COPD (chronic obstructive pulmonary disease). Whether IL-6 is directly involved or plays a bystander role in the pathophysiology of COPD remains unclear. Here we hypothesized that neutralizing circulating levels of IL-6 would modulate episodes of acute pulmonary inflammation following CS (cigarette smoke) exposure and virus-like challenges. For this purpose, we used a model where C57BL/6 mice were exposed to CS twice daily via a nose-only system, and concomitant periodic intranasal challenge with poly(I:C), a synthetic ligand for TLR3 (Toll-like receptor 3) that mimics the encounter with double stranded RNA that is carried by influenza-like viruses. This protocol recapitulates several aspects of acute pulmonary inflammation associated with COPD, including prominent airway neutrophilia, insensitivity to steroid treatment and increased levels of several inflammatory cytokines in BAL (bronchoalveolar lavage) samples. Although IL-6-deficient mice exposed to CS/poly(I:C) developed pulmonary inflammation similar to WT (wild-type) controls, WT mice exposed to CS/poly(I:C) and treated intraperitoneally with IL-6-neutralizing antibodies showed significantly lower blood counts of lymphocytes and monocytes, lower BAL levels of IL-6 and CXCL1 (CXC chemokine ligand 1)/KC (keratinocyte chemoattractant), as well as reduced numbers of BAL neutrophils, lymphocytes and macrophages. Our results thus indicate that the systemic neutralization of IL-6 significantly reduces CS/poly(I:C)-induced pulmonary inflammation, which may be a relevant approach to the treatment of episodes of acute pulmonary inflammation associated with COPD.

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Zhang, Hui, Yan-Fei Mao, Ying Zhao, Dun-Feng Xu, Yan Wang, Chu-Fan Xu, Wen-Wen Dong, et al. "Upregulation of Matrix Metalloproteinase-9 Protects against Sepsis-Induced Acute Lung Injury via Promoting the Release of Soluble Receptor for Advanced Glycation End Products." Oxidative Medicine and Cellular Longevity 2021 (February 10, 2021): 1–19. http://dx.doi.org/10.1155/2021/8889313.

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Dysregulation of matrix metalloproteinase- (MMP-) 9 is implicated in the pathogenesis of acute lung injury (ALI). However, it remains controversial whether MMP-9 improves or deteriorates acute lung injury of different etiologies. The receptor for advanced glycation end products (RAGE) plays a critical role in the pathogenesis of acute lung injury. MMPs are known to mediate RAGE shedding and release of soluble RAGE (sRAGE), which can act as a decoy receptor by competitively inhibiting the binding of RAGE ligands to RAGE. Therefore, this study is aimed at clarifying whether and how pulmonary knockdown of MMP-9 affected sepsis-induced acute lung injury as well as the release of sRAGE in a murine cecal ligation and puncture (CLP) model. The analysis of GEO mouse sepsis datasets GSE15379, GSE52474, and GSE60088 revealed that the mRNA expression of MMP-9 was significantly upregulated in septic mouse lung tissues. Elevation of pulmonary MMP-9 mRNA and protein expressions was confirmed in CLP-induced mouse sepsis model. Intratracheal injection of MMP-9 siRNA resulted in an approximately 60% decrease in pulmonary MMP-9 expression. It was found that pulmonary knockdown of MMP-9 significantly increased mortality of sepsis and exacerbated sepsis-associated acute lung injury. Pulmonary MMP-9 knockdown also decreased sRAGE release and enhanced sepsis-induced activation of the RAGE/nuclear factor-κB (NF-κB) signaling pathway, meanwhile aggravating sepsis-induced oxidative stress and inflammation in lung tissues. In addition, administration of recombinant sRAGE protein suppressed the activation of the RAGE/NF-κB signaling pathway and ameliorated pulmonary oxidative stress, inflammation, and lung injury in CLP-induced septic mice. In conclusion, our data indicate that MMP-9-mediated RAGE shedding limits the severity of sepsis-associated pulmonary edema, inflammation, oxidative stress, and lung injury by suppressing the RAGE/NF-κB signaling pathway via the decoy receptor activities of sRAGE. MMP-9-mediated sRAGE production may serve as a self-limiting mechanism to control and resolve excessive inflammation and oxidative stress in the lung during sepsis.

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Kaku, Shawn, Christopher D. Nguyen, Natalie N. Htet, Dominic Tutera, Juliana Barr, Harman S. Paintal, and Ware G. Kuschner. "Acute Respiratory Distress Syndrome: Etiology, Pathogenesis, and Summary on Management." Journal of Intensive Care Medicine 35, no. 8 (June 17, 2019): 723–37. http://dx.doi.org/10.1177/0885066619855021.

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The acute respiratory distress syndrome (ARDS) has multiple causes and is characterized by acute lung inflammation and increased pulmonary vascular permeability, leading to hypoxemic respiratory failure and bilateral pulmonary radiographic opacities. The acute respiratory distress syndrome is associated with substantial morbidity and mortality, and effective treatment strategies are limited. This review presents the current state of the literature regarding the etiology, pathogenesis, and management strategies for ARDS.

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Kearns, Mark T., Lea Barthel, Joseph M. Bednarek, Zulma X. Yunt, Peter M. Henson, and William J. Janssen. "Fas ligand-expressing lymphocytes enhance alveolar macrophage apoptosis in the resolution of acute pulmonary inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 1 (July 1, 2014): L62—L70. http://dx.doi.org/10.1152/ajplung.00273.2013.

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Apoptosis of alveolar macrophages and their subsequent clearance by neighboring phagocytes are necessary steps in the resolution of acute pulmonary inflammation. We have recently identified that activation of the Fas death receptor on the cell surface of macrophages drives macrophage apoptosis. However, the source of the cognate ligand for Fas (FasL) responsible for induction of alveolar macrophage apoptosis is not defined. Given their known role in the resolution of inflammation and ability to induce macrophage apoptosis ex vivo, we hypothesized that T lymphocytes represented a critical source of FasL. To address this hypothesis, C57BL/6J and lymphocyte-deficient (Rag-1−/−) mice were exposed to intratracheal lipopolysaccharide to induce pulmonary inflammation. Furthermore, utilizing mice expressing nonfunctional FasL, we adoptively transferred donor lymphocytes into inflamed lymphocyte-deficient mice to characterize the effect of lymphocyte-derived FasL on alveolar macrophage apoptosis in the resolution of inflammation. Herein, evidence is presented that lymphocytes expressing FasL enhance alveolar macrophage apoptosis during the resolution of LPS-induced inflammation. Moreover, lymphocyte induction of alveolar macrophage apoptosis results in contraction of the alveolar macrophage pool, which occurs in a FasL-dependent manner. Specifically, FasL-expressing CD8+T lymphocytes potently induce alveolar macrophage apoptosis and contraction of the alveolar macrophage pool. Together, these studies identify a novel role for CD8+T lymphocytes in the resolution of acute pulmonary inflammation.

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Kremserova, Silvie, Tomas Perecko, Karel Soucek, Anna Klinke, Stephan Baldus, Jason P. Eiserich, and Lukas Kubala. "Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/5219056.

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Systemic inflammation accompanying diseases such as sepsis affects primarily lungs and induces their failure. This remains the most common cause of sepsis induced mortality. While neutrophils play a key role in pulmonary failure, the mechanisms remain incompletely characterized. We report that myeloperoxidase (MPO), abundant enzyme in neutrophil granules, modulates the course of acute pulmonary inflammatory responses induced by intranasal application of lipopolysaccharide. MPO deficient mice had significantly increased numbers of airway infiltrated neutrophils compared to wild-type mice during the whole course of lung inflammation. This was accompanied by higher levels of RANTES in bronchoalveolar lavage fluid from the MPO deficient mice. Other markers of lung injury and inflammation, which contribute to recruitment of neutrophils into the inflamed lungs, including total protein and other selected proinflammatory cytokines did not significantly differ in bronchoalveolar lavage fluid from the wild-type and the MPO deficient mice. Interestingly, MPO deficient neutrophils revealed a decreased rate of cell death characterized by phosphatidylserine surface expression. Collectively, the importance of MPO in regulation of pulmonary inflammation, independent of its putative microbicidal functions, can be potentially linked to MPO ability to modulate the life span of neutrophils and to affect accumulation of chemotactic factors at the inflammatory site.

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Lee, Soung-Min, Ha Young Park, Young-Sill Suh, Eun Hye Yoon, Juyang Kim, Won Hee Jang, Won-Sik Lee, et al. "Inhibition of acute lethal pulmonary inflammation by the IDO–AhR pathway." Proceedings of the National Academy of Sciences 114, no. 29 (July 3, 2017): E5881—E5890. http://dx.doi.org/10.1073/pnas.1615280114.

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The lung is a prototypic organ that was evolved to reduce immunopathology during the immune response to potentially hazardous endogenous and exogenous antigens. In this study, we show that donor CD4+ T cells transiently induced expression of indoleamine 2,3-dioxygenase (IDO) in lung parenchyma in an IFN-γ–dependent manner early after allogeneic hematopoietic stem cell transplantation (HSCT). Abrogation of host IDO expression by deletion of the IDO gene or the IFN-γ gene in donor T cells or by FK506 treatment resulted in acute lethal pulmonary inflammation known as idiopathic pneumonia syndrome (IPS). Interestingly, IL-6 strongly induced IDO expression in an IFN-γ–independent manner when deacetylation of STAT3 was inhibited. Accordingly, a histone deacetylase inhibitor (HDACi) could reduce IPS in the state where IFN-γ expression was suppressed by FK506. Finally, l-kynurenine produced by lung epithelial cells and alveolar macrophages during IPS progression suppresses the inflammatory activities of lung epithelial cells and CD4+ T cells through the aryl hydrocarbon receptor pathway. Taken together, our results reveal that IDO is a critical regulator of acute pulmonary inflammation and that regulation of IDO expression by HDACi may be a therapeutic approach for IPS after HSCT.

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Lavrova, Anastasia, Diljara Esmedljaeva, Vitaly Belik, and Eugene Postnikov. "Matrix Metalloproteinases as Markers of Acute Inflammation Process in the Pulmonary Tuberculosis." Data 4, no. 4 (October 5, 2019): 137. http://dx.doi.org/10.3390/data4040137.

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The main factors of pathogenesis in the pulmonary tuberculosis are not only the bacterial virulence and sensitivity of the host immune system to the pathogen, but also the degree of destruction of the lung tissue. Such destruction processes lead to the development of caverns, in most cases requiring surgical interventions besides the drug therapy. Identification of special biochemical markers allowing to assess the necessity of surgery or therapy prolongation remains a challenge. We consider promising markers—metalloproteinases—analyzing the data obtained from patients with pulmonary tuberculosis infected by different strains of Mycobacterium tuberculosis. We argue that the presence of drug-resistant strains in lungs leading to complicated clinical prognosis could be justified not only by the difference in medians of biomarkers concentration (as determined by the Mann–Whitney test for small samples), but also by the qualitative difference in their probability distributions (as detected by the Kolmogorov–Smirnov test). Our results and the provided raw data could be used for further development of precise biochemical data-based diagnostic and prognostic tools for pulmonary tuberculosis.

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Revenstorff, Julian, Nadine Ludwig, Annika Hilger, Sina Mersmann, Martin Lehmann, Julia Chiara Grenzheuser, Marina Kardell, et al. "Role of S100A8/A9 in Platelet–Neutrophil Complex Formation during Acute Inflammation." Cells 11, no. 23 (December 6, 2022): 3944. http://dx.doi.org/10.3390/cells11233944.

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Acute respiratory distress syndrome (ARDS) due to pulmonary infections is associated with high morbidity and mortality. Upon inflammation, the alarmin S100A8/A9 is released and stimulates neutrophil recruitment mainly via binding to Toll-like receptor 4 (TLR4). TLR4 is also expressed on platelets, which modulate the immune response through direct interaction with leukocytes. In a murine model of Klebsiella pneumoniae-induced pulmonary inflammation, global S100A9 deficiency resulted in diminished neutrophil recruitment into the lung alveoli and neutrophil accumulation in the intravascular space, indicating an impaired neutrophil migration. A lack of TLR4 on platelets resulted in reduced neutrophil counts in the whole lung, emphasising the impact of TLR4-mediated platelet activity on neutrophil behaviour. Flow cytometry-based analysis indicated elevated numbers of platelet–neutrophil complexes in the blood of S100A9−/− mice. Intravital microscopy of the murine cremaster muscle confirmed these findings and further indicated a significant increase in neutrophil–platelet complex formation in S100A9−/− mice, which was reversed by administration of the S100A8/A9 tetramer. An in vitro bilayer assay simulated the murine alveolar capillary barrier during inflammation and validated significant differences in transmigration behaviour between wild-type and S100A9−/− neutrophils. This study demonstrates the role of S100A8/A9 during platelet–neutrophil interactions and neutrophil recruitment during pulmonary inflammation.

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Perl, Mario, Chun-Shiang Chung, Ulrike Perl, Joanne Lomas-Neira, Monique de Paepe, William G. Cioffi, and Alfred Ayala. "Fas-induced Pulmonary Apoptosis and Inflammation during Indirect Acute Lung Injury." American Journal of Respiratory and Critical Care Medicine 176, no. 6 (September 15, 2007): 591–601. http://dx.doi.org/10.1164/rccm.200611-1743oc.

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de Campos, Tercio, Jessica Deree, Joilson O. Martins, William H. Loomis, Edna Shenvi, James G. Putnam, and Raul Coimbra. "Pentoxifylline Attenuates Pulmonary Inflammation and Neutrophil Activation in Experimental Acute Pancreatitis." Pancreas 37, no. 1 (July 2008): 42–49. http://dx.doi.org/10.1097/mpa.0b013e3181612d19.

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Ilves, Marit, Sara Vilske, Kukka Aimonen, Hanna K. Lindberg, Saila Pesonen, Irene Wedin, Markus Nuopponen, et al. "Nanofibrillated cellulose causes acute pulmonary inflammation that subsides within a month." Nanotoxicology 12, no. 7 (May 30, 2018): 729–46. http://dx.doi.org/10.1080/17435390.2018.1472312.

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Fernandez-Bustamante, A., R. B. Easley, M. Fuld, D. Mulreany, D. Chon, J. F. Lewis, and B. A. Simon. "Regional pulmonary inflammation in an endotoxemic ovine acute lung injury model." Respiratory Physiology & Neurobiology 183, no. 2 (August 2012): 149–58. http://dx.doi.org/10.1016/j.resp.2012.06.015.

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Mackarel, A. Jill, Kenneth J. Russell, Clodagh M. Ryan, Shirley J. Hislip, Jacqueline C. Rendall, Muiris X. FitzGerald, and Clare M. O’Connor. "CD18 Dependency of Transendothelial Neutrophil Migration Differs During Acute Pulmonary Inflammation." Journal of Immunology 167, no. 5 (September 1, 2001): 2839–46. http://dx.doi.org/10.4049/jimmunol.167.5.2839.

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Haegens, Astrid, Annemie M. Schols, Stefan H. Gorissen, Anon L. van Essen, Frank Snepvangers, Douglas A. Gray, Steven E. Shoelson, and Ramon C. Langen. "NF-κB activation and polyubiquitin conjugation are required for pulmonary inflammation-induced diaphragm atrophy." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 1 (January 1, 2012): L103—L110. http://dx.doi.org/10.1152/ajplung.00084.2011.

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Loss of diaphragm muscle strength in inflammatory lung disease contributes to mortality and is associated with diaphragm fiber atrophy. Ubiquitin (Ub) 26S-proteasome system (UPS)-dependent protein breakdown, which mediates muscle atrophy in a number of physiological and pathological conditions, is elevated in diaphragm muscle of patients with chronic obstructive pulmonary disease. Nuclear factor kappa B (NF-κB), an essential regulator of many inflammatory processes, has been implicated in the regulation of poly-Ub conjugation of muscle proteins targeted for proteolysis by the UPS. Here, we test if NF-κB activation in diaphragm muscle and subsequent protein degradation by the UPS are required for pulmonary inflammation-induced diaphragm atrophy. Acute pulmonary inflammation was induced in mice by intratracheal lipopolysaccharide instillation. Fiber cross-sectional area, ex vivo tyrosine release, protein poly-Ub conjugation, and inflammatory signaling were determined in diaphragm muscle. The contribution of NF-κB or the UPS to diaphragm atrophy was assessed in mice with intact or genetically repressed NF-κB signaling or attenuated poly-Ub conjugation, respectively. Acute pulmonary inflammation resulted in diaphragm atrophy measured by reduced muscle fiber cross-sectional area. This was accompanied by diaphragm NF-κB activation, and proteolysis, measured by tyrosine release from the diaphragm. Poly-Ub conjugation was increased in diaphragm, as was the expression of muscle-specific E3 Ub ligases. Genetic suppression of poly-Ub conjugation prevented inflammation-induced diaphragm muscle atrophy, as did muscle-specific inhibition of NF-κB signaling. In conclusion, the present study is the first to demonstrate that diaphragm muscle atrophy, resulting from acute pulmonary inflammation, requires NF-κB activation and UPS-mediated protein degradation.

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Gibson Alves, Thiago G., Ana P. R. Sierra, Renilson Moraes Ferreira, Maysa A. R. Brandão-Rangel, Anamei Silva-Reis, Tiago A. De Lima, Luis V. F. De Oliveira, et al. "Acute Effects of Marathon Running on Lung Function, Lung Mechanics, and Inflammation." European Journal of Sport Sciences 1, no. 6 (November 7, 2022): 13–18. http://dx.doi.org/10.24018/ejsport.2022.1.6.40.

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This study investigated the influence of the marathon on lung function, mechanics, and pulmonary inflammation. Twenty-eight male amateur marathon runners (42.1±6.2 years) were evaluated before and immediately after marathon. Pulmonary function and mechanics were assessed using spirometry and impulse oscillometry, respectively, whereas fatigue of the respiratory muscles by manovacuometry and lung inflammation by fractional exhaled nitric oxide (FeNO). Marathon induced a significant reduction in the lung function as compared to baseline values: FVC (4.81±0.72 vs 4.67±0.62, p=0.0095), VC IN (4.81±0.72 vs 4.67±0.62, p=0.009), FEV1 (3.83±0.62 vs 3.72±0.59, p=0.0232), and FEV6 (4.87±0.68 vs 4.57±0.63, p=0.0006), as well as an impairment in the lung mechanics in comparison to baseline values: reduced pulmonary impedance (Z5Hz; 2.96±1.36 vs 2.67±1.11; p=0.0305), reduced resistance of the whole respiratory system (R5Hz; 2.76±1.27 vs 2.5±1.08; p=0.0388) and pulmonary reactance (X5Hz; -1.05±0.55 vs -0.91±0.36; p=0.0101) and of resistance of proximal airways (R5Hz; 1.26±0.73 vs 1.06±0.86; p= 0.0377). In addition, maximal inspiratory (MIP; 94.14±41.88 vs 72.52±25.50; p=0.0023) and expiratory (MEP; 99.31±31.84 vs 91.29±19.94; p=0.0454) pressures, as well as FeNO levels were lower after the marathon than values pre-marathon (p=0.0359). Marathon running causes an acute disturbance in lung function and mechanics and compromises respiratory muscle strength.

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Johnston, Richard A., Todd A. Theman, Raya D. Terry, Erin S. Williams, and Stephanie A. Shore. "Pulmonary responses to acute ozone exposure in fasted mice: effect of leptin administration." Journal of Applied Physiology 102, no. 1 (January 2007): 149–56. http://dx.doi.org/10.1152/japplphysiol.00300.2006.

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Leptin is a satiety hormone that also has proinflammatory effects, including augmentation of ozone-induced pulmonary inflammation. The purpose of this study was to determine whether reductions in endogenous levels of leptin can attenuate pulmonary responses to ozone. To reduce serum leptin, we fasted mice overnight before ozone exposure. Fasting caused a marked reduction in serum leptin to approximately one-sixth the levels observed in fed mice, and continuous infusion of leptin via Alzet micro-osmotic pumps restored serum leptin to, but not above, fed levels. Ozone exposure (2 ppm for 3 h) caused a significant, ∼40% increase in pulmonary resistance ( P < 0.01) and increased airway responsiveness in fasted but not in fed mice. The increased effect of ozone on pulmonary mechanics and airway responsiveness in fasted mice was not observed when leptin was restored via continuous infusion. Ozone exposure caused pulmonary inflammation, as evident by increases in bronchoalveolar lavage cells, protein, and soluble tumor necrosis factor receptors. There was no effect of fasting status on ozone-induced changes in the bronchoalveolar lavage inflammatory profile, and leptin treatment did not alter these responses. Our results indicate that fasting augments ozone-induced changes in pulmonary mechanics and airway responsiveness in mice. These effects of fasting are the result of declines in serum leptin. The mechanistic basis for this protective effect of leptin in fasted mice remains to be determined but is not related to effects on ozone-induced inflammation.

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Wonnenberg, Bodo, Christopher Jungnickel, Anja Honecker, Lisa Wolf, Meike Voss, Markus Bischoff, Thomas Tschernig, Christian Herr, Robert Bals, and Christoph Beisswenger. "IL-17A attracts inflammatory cells in murine lung infection with P. aeruginosa." Innate Immunity 22, no. 8 (September 22, 2016): 620–25. http://dx.doi.org/10.1177/1753425916668244.

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IL-17A-dependent immunity is of importance in the protection against extracellular bacterial pathogens. However, IL-17A is also suggested to mediate the pathogenesis of lung diseases, such as acute respiratory distress syndrome. Here, we studied the role of IL-17A in a mouse model of acute pneumonia. IL-17A mediated the expression of keratinocyte-derived chemokine (KC) and the recruitment of inflammatory cells in mice infected with a sub-lethal dose of Pseudomonas aeruginosa. IL-17A deficiency protected mice from lethal P. aeruginosa lung infection. A sub-lethal infection with Streptococcus pneumoniae resulted in increased bacterial burden associated with increased pulmonary inflammation. Thus, the type of infectious bacteria seemed to influence the way in which IL-17A functions during pulmonary infection. Reducing pulmonary inflammation by targeting IL-17A may be a therapeutic option in acute P. aeruginosa pneumonia.

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Carraway, Martha, Thomas Ortel, Claude Piantadosi, and Karen Welty-Wolf. "Coagulation and Inflammation in Acute Lung Injury." Thrombosis and Haemostasis 88, no. 07 (2002): 17–25. http://dx.doi.org/10.1055/s-0037-1613147.

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SummaryThe acute respiratory distress syndrome (ARDS) is a severe lung injury in patients with sepsis and other acute inflammatory insults, which is characterized by fibrin deposition in the pulmonary parenchyma, vasculature, and airspaces. Recent evidence suggests that progressive ARDS is closely linked to activation of inflammation and coagulation. Coagulation becomes activated by circulating endotoxin or bacteria, and a procoagulant state develops in the vascular and the alveolar compartments of the lung. This state is Tissue Factor (TF)-dependent and associated with increased elaboration of inflammatory cytokines. A similar procoagulant state is found in bronchoalveolar lavage of patients with ARDS, suggesting that extravascular coagulation contributes to lung inflammation. TF and other coagulation proteins, including Factor Xa, thrombin, and fibrin, also contribute to the pathogenesis of acute lung injury through multi-level interactions with inflammatory effectors, in which these proteins coordinately act as regulators of tissue injury responses. Each coagulation protein has direct and independent effects on inflammatory events that influences lung injury through changes in cytokine elaboration, inflammatory cell migration and activation, surfactant function, and repair mechanisms. New interventional strategies directed at procoagulant activity highlight the importance of the coagulation system to acute lung injury and suggest that blockade of initiation of coagulation may have therapeutic benefit in patients with ARDS.

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Karki, Pratap, and Anna A. Birukova. "Substrate stiffness-dependent exacerbation of endothelial permeability and inflammation: mechanisms and potential implications in ALI and PH (2017 Grover Conference Series)." Pulmonary Circulation 8, no. 2 (April 2018): 204589401877304. http://dx.doi.org/10.1177/2045894018773044.

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The maintenance of endothelial barrier integrity is absolutely essential to prevent the vascular leak associated with pneumonia, pulmonary edema resulting from inhalation of toxins, acute elevation to high altitude, traumatic and septic lung injury, acute lung injury (ALI), and its life-threatening complication, acute respiratory distress syndrome (ARDS). In addition to the long-known edemagenic and inflammatory agonists, emerging evidences suggest that factors of endothelial cell (EC) mechanical microenvironment such as blood flow, mechanical strain of the vessel, or extracellular matrix stiffness also play an essential role in the control of endothelial permeability and inflammation. Recent studies from our group and others have demonstrated that substrate stiffening causes endothelial barrier disruption and renders EC more susceptible to agonist-induced cytoskeletal rearrangement and inflammation. Further in vivo studies have provided direct evidence that proinflammatory stimuli increase lung microvascular stiffness which in turn exacerbates endothelial permeability and inflammation and perpetuates a vicious circle of lung inflammation. Accumulating evidence suggests a key role for RhoA GTPases signaling in stiffness-dependent mechanotransduction mechanisms defining EC permeability and inflammatory responses. Vascular stiffening is also known to be a key contributor to other cardiovascular diseases such as arterial pulmonary hypertension (PH), although the precise role of stiffness in the development and progression of PH remains to be elucidated. This review summarizes the current understanding of stiffness-dependent regulation of pulmonary EC permeability and inflammation, and discusses potential implication of pulmonary vascular stiffness alterations at macro- and microscale in development and modulation of ALI and PH.

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Vella, Giovanna, Felix Ritzmann, Lisa Wolf, Andreas Kamyschnikov, Hannah Stodden, Christian Herr, Hortense Slevogt, Robert Bals, and Christoph Beisswenger. "IL-17C contributes to NTHi-induced inflammation and lung damage in experimental COPD and is present in sputum during acute exacerbations." PLOS ONE 16, no. 1 (January 7, 2021): e0243484. http://dx.doi.org/10.1371/journal.pone.0243484.

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Neutrophilic inflammation results in loss of lung function in chronic obstructive pulmonary disease (COPD). Gram-negative bacteria, such as nontypeable Haemophilus influenzae (NTHi), trigger acute exacerbations of COPD (AECOPD) and contribute to chronic lung inflammation. The pro-inflammatory cytokine interleukin-17C (IL-17C) is expressed by airway epithelial cells and regulates neutrophilic chemotaxis. Here, we explored the function of IL-17C in NTHi- and cigarette smoke (CS)-induced models of COPD. Neutrophilic inflammation and tissue destruction were decreased in lungs of IL-17C-deficient mice (Il-17c-/-) chronically exposed to NTHi. Numbers of pulmonary neutrophils were decreased in Il-17c-/- mice after acute exposure to the combination of NTHi and CS. However, Il-17c-/- mice were not protected from CS-induced lung inflammation. In a preliminary patient study, we show that IL-17C is present in sputum samples obtained during AECOPD and associates with disease severity. Concentrations of IL-17C were significantly increased during advanced COPD (GOLD III/IV) compared to moderate COPD (GOLD I/II). Concentrations of IL-17A and IL-17E did not associate with disease severity. Our data suggest that IL-17C promotes harmful pulmonary inflammation triggered by bacteria in COPD.

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Kim, Hye-Yoom, Jung-Joo Yoon, Dae-Sung Kim, Dae-Gill Kang, and Ho-Sub Lee. "YG-1 Extract Improves Acute Pulmonary Inflammation by Inducing Bronchodilation and Inhibiting Inflammatory Cytokines." Nutrients 13, no. 10 (September 28, 2021): 3414. http://dx.doi.org/10.3390/nu13103414.

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YG-1 extract used in this study is a mixture of Lonicera japonica, Arctic Fructus, and Scutellariae Radix. The present study was designed to investigate the effect of YG-1 extract on bronchodilatation (ex vivo) and acute bronchial and pulmonary inflammation relief (in vivo). Ex vivo: The bronchodilation reaction was confirmed by treatment with YG-1 concentration-accumulation (0.01, 0.03, 0.1, 0.3, and 1 mg/mL) in the bronchial tissue ring pre-contracted by acetylcholine (10 μM). As a result, YG-1 extract is considered to affect bronchodilation by increased cyclic adenosine monophosphate, cAMP) levels through the β2-adrenergic receptor. In vivo: experiments were performed in C57BL/6 mice were divided into the following groups: control group; PM2.5 (fine particulate matter)-exposed group (PM2.5, 200 μg/kg/mL saline); and PM2.5-exposed + YG-1 extract (200 mg/kg/day) group. The PM2.5 (200 μg/kg/mL saline) was exposed for 1 h for 5 days using an ultrasonic nebulizer aerosol chamber to instill fine dust in the bronchi and lungs, thereby inducing acute lung and bronchial inflammation. From two days before PM2.5 exposure, YG-1 extract (200 mg/kg/day) was administered orally for 7 days. The PM2.5 exposure was involved in airway remodeling and inflammation, suggesting that YG-1 treatment improves acute bronchial and pulmonary inflammation by inhibiting the inflammatory cytokines (NLRP3/caspase-1 pathway). The application of YG-1 extract with broncho-dilating effect to acute bronchial and pulmonary inflammation animal models has great significance in developing therapeutic agents for respiratory diseases. Therefore, these results can provide essential data for the development of novel respiratory symptom relievers. Our study provides strong evidence that YG-1 extracts reduce the prevalence of respiratory symptoms and the incidence of non-specific lung diseases and improve bronchial and lung function.

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Slocombe, R. F., and D. O. Slauson. "Invasive Pulmonary Aspergillosis of Horses: An Association with Acute Enteritis." Veterinary Pathology 25, no. 4 (July 1988): 277–81. http://dx.doi.org/10.1177/030098588802500405.

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Invasive pulmonary aspergillosis was identified in 19 horses. In 16 cases mycotic lesions were associated with enterocolitis; 14 cases appeared to result from Salmonella infection. Pulmonary lesions included multifocal areas of acute necrosis, leukocytoclastic vasculitis, and thrombosis with fibrinosuppurative inflammation surrounding mycelial masses. Thromboemboli with fungi were in the brain and kidneys of three cases. Factors which appeared to predispose to pulmonary aspergillosis included corticosteroid therapy, disseminated neoplasms, hepatitis, pleuritis, and peritonitis. This study suggests that immunocompromise and invasion of Aspergillus sp. from damaged intestine are more important in causing equine pulmonary aspergillosis than inhalation of spores.

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Rittchen, Sonja, Katharina Jandl, Ilse Lanz, Bernhard Reiter, Nerea Ferreirós, Daniel Kratz, Jörg Lindenmann, et al. "Monocytes and Macrophages Serve as Potent Prostaglandin D2 Sources during Acute, Non-Allergic Pulmonary Inflammation." International Journal of Molecular Sciences 22, no. 21 (October 28, 2021): 11697. http://dx.doi.org/10.3390/ijms222111697.

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Acute respiratory inflammation, most commonly resulting from bacterial or viral infection, is one of the leading causes of death and disability worldwide. The inflammatory lipid mediator prostaglandin D2 (PGD2) and its rate-limiting enzyme, hematopoietic PGD synthase (hPGDS), are well-known drivers of allergic pulmonary inflammation. Here, we sought to investigate the source and role of hPGDS-derived PGD2 in acute pulmonary inflammation. Murine bronchoalveolar monocytes/macrophages from LPS- but not OVA-induced lung inflammation released significant amounts of PGD2. Accordingly, human monocyte-derived macrophages expressed high basal levels of hPGDS and released significant levels of PGD2 after LPS/IFN-γ, but not IL-4 stimulation. Human peripheral blood monocytes secreted significantly more PGD2 than monocyte-derived macrophages. Using human precision-cut lung slices (PCLS), we observed that LPS/IFN-γ but not IL-4/IL-13 drive PGD2 production in the lung. HPGDS inhibition prevented LPS-induced PGD2 release by human monocyte-derived macrophages and PCLS. As a result of hPGDS inhibition, less TNF-α, IL-6 and IL-10 could be determined in PCLS-conditioned medium. Collectively, this dataset reflects the time-dependent release of PGD2 by human phagocytes, highlights the importance of monocytes and macrophages as PGD2 sources and suggests that hPGDS inhibition might be a potential therapeutic option for acute, non-allergic lung inflammation.

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Zambelli, Vanessa, Laura Rizzi, Paolo Delvecchio, Elena Bresciani, Emanuele Rezoagli, Laura Molteni, Ramona Meanti, et al. "Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury." Drug Target Insights 15 (November 21, 2021): 26–33. http://dx.doi.org/10.33393/dti.2021.2347.

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Introduction: Acute respiratory distress syndrome (ARDS) is an acute form of diffuse lung injury characterized by (i) an intense inflammatory response, (ii) increased pulmonary vascular permeability, and (iii) the loss of respiratory pulmonary tissue. In this article we explore the therapeutic potential of hexarelin, a synthetic hexapeptide growth hormone secretagogue (GHS), in an experimental model of ARDS. Hexarelin has anti-inflammatory properties and demonstrates cardiovascular-protective activities including the inhibition of cardiomyocyte apoptosis and cardiac fibrosis, both of which may involve the angiotensin-converting enzyme (ACE) system. Methods: In our experimental model, ARDS was induced by the instillation of 100 mM HCl into the right bronchus; these mice were treated with hexarelin (320 μg/kg, ip) before (Pre) or after (Post) HCl challenge, or with vehicle. Respiratory system compliance, blood gas analysis, and differential cell counts in a selective bronchoalveolar lavage (BAL) were determined 6 or 24 hours after HCl instillation. In an extended study, mice were observed for a subsequent 14 days in order to assess lung fibrosis. Results: Hexarelin induced a significant improvement in lung compliance and a reduction of the number of total immune cells in BAL 24 hours after HCl instillation, accompanied with a lower recruitment of neutrophils compared with the vehicle group. At day 14, hexarelin-treated mice presented with less pulmonary collagen deposition compared with vehicle-treated controls. Conclusions: Our data suggest that hexarelin can inhibit the early phase of the inflammatory response in a murine model of HCl-induced ARDS, thereby blunting lung remodeling processes and fibrotic development.

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Harrod, Kevin S., Amber D. Mounday, Barry R. Stripp, and Jeffrey A. Whitsett. "Clara cell secretory protein decreases lung inflammation after acute virus infection." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 5 (November 1, 1998): L924—L930. http://dx.doi.org/10.1152/ajplung.1998.275.5.l924.

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Clara cell secretory protein (CCSP) is an abundant 10-kDa polypeptide synthesized and secreted primarily by nonciliated bronchiolar epithelial cells in the mammalian lung. To determine the potential role of CCSP in pulmonary inflammation after acute viral infection, CCSP gene-targeted {CCSP-deficient [CCSP(−/−)]} mice were exposed to a recombinant E1- and E3-deficient adenoviral vector, Av1Luc1, intratracheally. Lung inflammation was markedly increased in CCSP(−/−) mice compared with wild-type control mice and was associated with an increased number of polymorphonuclear cell infiltrates and epithelial cell injury in both conducting airways and alveolar regions. Histological evidence of pulmonary inflammation in CCSP(−/−) mice was associated with increased production of cytokine (interleukin-1β and -6 and tumor necrosis factor-α) mRNA and protein, as well as chemokine (macrophage inflammatory protein-1α and -2 and monocyte chemoattractant protein-1) mRNA expression within the lung in response to adenoviral infection. Adenoviral-mediated gene transfer was decreased in CCSP(−/−) mice relative to wild-type mice as measured by luciferase enzyme activity in lung homogenates. The present study suggests that CCSP is involved in modulating lung inflammation during viral infection and supports a role for CCSP in lung host defense.

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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, parasites are taken up by resident macrophages. This is associated with the transient activation of resident macrophages and the release of chemokines that recruit large numbers of CD11b+Ly6C+ blood monocytes. Flow cytometry results suggest that later in infection resident lung macrophages take on a regulatory phenotype, while the recruited monocytes undergo activation, differentiation into macrophages and are responsible for the majority of parasite clearance within the lungs. Administration of a blocking monoclonal antibody (anti-CD11b; 5C6) diminishes the homing of monocytes to the lungs, resulting in decreased parasite uptake. We propose that both myeloid populations control pulmonary inflammation through the clearance of sequestered parasites within the pulmonary microvasculature as well as the regulation of pro-inflammatory processes within the lung environment.

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Kotnala, Sudhir, Yerin Kim, Charu Rajput, Hymavathi Reddyvari, Sudhir Bolla, Nathaniel T. Marchetti, Beata Kosmider, Karim Bahmed, and Umadevi S. Sajjan. "Contribution of dipeptidyl peptidase 4 to non-typeable Haemophilus influenzae-induced lung inflammation in COPD." Clinical Science 135, no. 17 (September 1, 2021): 2067–83. http://dx.doi.org/10.1042/cs20210099.

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Abstract Dipeptidyl peptidase 4 (DPP4) expression is increased in the lungs of chronic obstructive pulmonary disease (COPD). DPP4 is known to be associated with inflammation in various organs, including LPS-induced acute lung inflammation. Since non-typeable Haemophilus influenzae (NTHi) causes acute exacerbations in COPD patients, we examined the contribution of DPP4 in NTHi-induced lung inflammation in COPD. Pulmonary macrophages isolated from COPD patients showed higher expression of DPP4 than the macrophages isolated from normal subjects. In response to NTHi infection, COPD, but not normal macrophages show a further increase in the expression of DPP4. COPD macrophages also showed higher expression of IL-1β, and CCL3 responses to NTHi than normal, and treatment with DPP4 inhibitor, diprotin A attenuated this response. To examine the contribution of DPP4 in NTHi-induced lung inflammation, COPD mice were infected with NTHi, treated with diprotin A or PBS intraperitoneally, and examined for DPP4 expression, lung inflammation, and cytokine expression. Mice with COPD phenotype showed increased expression of DPP4, which increased further following NTHi infection. DPP4 expression was primarily observed in the infiltrated inflammatory cells. NTHi-infected COPD mice also showed sustained neutrophilic lung inflammation and expression of CCL3, and this was inhibited by DPP4 inhibitor. These observations indicate that enhanced expression of DPP4 in pulmonary macrophages may contribute to sustained lung inflammation in COPD following NTHi infection. Therefore, inhibition of DPP4 may reduce the severity of NTHi-induced lung inflammation in COPD.

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Felton, Jennifer M., Rodger Duffin, Calum T. Robb, Siobhan Crittenden, Stephen M. Anderton, Sarah E. M. Howie, Moira K. B. Whyte, Adriano G. Rossi, and Chengcan Yao. "Facilitation of IL-22 production from innate lymphoid cells by prostaglandin E2 prevents experimental lung neutrophilic inflammation." Thorax 73, no. 11 (March 24, 2018): 1081–84. http://dx.doi.org/10.1136/thoraxjnl-2017-211097.

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Acute lung injury is a neutrophil-dominant, life-threatening disease without effective therapies and better understanding of the pathophysiological mechanisms involved is an urgent need. Here we show that interleukin (IL)-22 is produced from innate lymphoid cells (ILC) and is responsible for suppression of experimental lung neutrophilic inflammation. Blocking prostaglandin E2 (PGE2) synthesis reduces lung ILCs and IL-22 production, resulting in exacerbation of lung neutrophilic inflammation. In contrast, activation of the PGE2 receptor EP4 prevents acute lung inflammation. We thus demonstrate a mechanism for production of innate IL-22 in the lung during acute injury, highlighting potential therapeutic strategies for control of lung neutrophilic inflammation by targeting the PGE2/ILC/IL-22 axis.

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Chen, Hui, Longhuan Zeng, Guangwei Jiang, and Qian Liu. "Mechanism of the Protective Effect of Sesamin on Sepsis-Induced Acute Lung Injury." Current Topics in Nutraceutical Research 19, no. 2 (September 2, 2020): 211–16. http://dx.doi.org/10.37290/ctnr2641-452x.19:211-216.

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Sepsis is the syndrome of systemic inflammatory response caused by infection. Over 20 million people worldwide suffer from sepsis each year, of whom about 6 million die, with a case-fatality rate of more than 25%. Therefore, to develop a rational plan for the management of sepsis, there is an urgent need to understand the mechanism of pathogenesis. Sesamin is a kind of sesame lignin isolated from sesame that exhibits multiple biological functions including antiviral, antidyslipidemic, and antihypertensive to name a few. An antioxidant and anti-inflammatory activity of sesamin appears to be a common denominator in all of its biologic activities. However, the mechanism of sesamin on septic-induced acute pulmonary inflammation still needs further study. Herein, we have established a sepsis model of C57BL/6 mice by cecal ligation and perforation. Using this model, we have shown that sesamin could reduce the levels of several inflammatory factors as well as oxidative stress response. Furthermore, sesamin could repress NLRP3 inflammasome and activate Nrf2/HO-1 pathway, and further inhibit acute pulmonary inflammation. This study reveals the mechanism of the diminution of septic-induced acute pulmonary inflammation by sesamin. This opens a theoretical basis for the development of drugs for treatment of sepsis.

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Chen, Siyao, Yaqian Huang, Zhiwei Liu, Wen Yu, Heng Zhang, Kun Li, Xiaoqi Yu, et al. "Sulphur dioxide suppresses inflammatory response by sulphenylating NF-κB p65 at Cys38 in a rat model of acute lung injury." Clinical Science 131, no. 21 (October 27, 2017): 2655–70. http://dx.doi.org/10.1042/cs20170274.

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The present study was designed to investigate whether endogenous sulphur dioxide (SO2) controlled pulmonary inflammation in a rat model of oleic acid (OA)-induced acute lung injury (ALI). In this model, adenovirus expressing aspartate aminotransferase (AAT) 1 was delivered to the lungs, and the levels of SO2 and proinflammatory cytokines in rat lung tissues were measured. In the human alveolar epithelial cell line A549, the nuclear translocation and DNA binding activities of wild-type (wt) and C38S (cysteine-to-serine mutation at p65 Cys38) NF-κB p65 were detected. GFP-tagged C38S p65 was purified from HEK 293 cells and the sulphenylation of NF-κB p65 was studied. OA caused a reduction in SO2/AAT pathway activity but increased pulmonary inflammation and ALI. However, either the presence of SO2 donor, a combination of Na2SO3 and NaHSO3, or AAT1 overexpression in vivo successfully blocked OA-induced pulmonary NF-κB p65 phosphorylation and consequent inflammation and ALI. Either treatment with an SO2 donor or overexpression of AAT1 down-regulated OA-induced p65 activity, but AAT1 knockdown in alveolar epithelial cells mimicked OA-induced p65 phosphorylation and inflammation in vitro. Mechanistically, OA promoted NF-κB nuclear translocation, DNA binding activity, recruitment to the intercellular cell adhesion molecule (ICAM)-1 promoter, and consequent inflammation in epithelial cells; these activities were reduced in the presence of an SO2 donor. Furthermore, SO2 induced sulphenylation of p65, which was blocked by the C38S mutation on p65 in epithelial cells. Hence, down-regulation of SO2/AAT is involved in pulmonary inflammation during ALI. Furthermore, SO2 suppressed inflammation by sulphenylating NF-κB p65 at Cys38.

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Journal articles on the topic 'Pulmonary acute inflammation'

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