Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation
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 myelo...
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Series: | Oxidative Medicine and Cellular Longevity |
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doaj-dbf77608b5834ce292d86eb0dd68bd9c2020-11-25T01:37:03ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942016-01-01201610.1155/2016/52190565219056Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary InflammationSilvie Kremserova0Tomas Perecko1Karel Soucek2Anna Klinke3Stephan Baldus4Jason P. Eiserich5Lukas Kubala6Department of Free Radical Pathophysiology, Institute of Biophysics, Academy of Sciences of the Czech Republic, 61265 Brno, Czech RepublicDepartment of Free Radical Pathophysiology, Institute of Biophysics, Academy of Sciences of the Czech Republic, 61265 Brno, Czech RepublicInternational Clinical Research Center, Center of Biomolecular and Cellular Engineering, St. Anne’s University Hospital Brno, 65691 Brno, Czech RepublicInternational Clinical Research Center, Center of Biomolecular and Cellular Engineering, St. Anne’s University Hospital Brno, 65691 Brno, Czech RepublicHeart Center, University of Cologne, 50937 Cologne, GermanyDepartment of Internal Medicine, School of Medicine, University of California, Davis, CA 95616, USADepartment of Free Radical Pathophysiology, Institute of Biophysics, Academy of Sciences of the Czech Republic, 61265 Brno, Czech RepublicSystemic 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.http://dx.doi.org/10.1155/2016/5219056 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Silvie Kremserova Tomas Perecko Karel Soucek Anna Klinke Stephan Baldus Jason P. Eiserich Lukas Kubala |
spellingShingle |
Silvie Kremserova Tomas Perecko Karel Soucek Anna Klinke Stephan Baldus Jason P. Eiserich Lukas Kubala Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation Oxidative Medicine and Cellular Longevity |
author_facet |
Silvie Kremserova Tomas Perecko Karel Soucek Anna Klinke Stephan Baldus Jason P. Eiserich Lukas Kubala |
author_sort |
Silvie Kremserova |
title |
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation |
title_short |
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation |
title_full |
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation |
title_fullStr |
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation |
title_full_unstemmed |
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation |
title_sort |
lung neutrophilia in myeloperoxidase deficient mice during the course of acute pulmonary inflammation |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2016-01-01 |
description |
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. |
url |
http://dx.doi.org/10.1155/2016/5219056 |
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