2016
Kremserova, Silvie; Perecko, Tomas; Soucek, Karel; Klinke, Anna; Baldus, Stephan; Eiserich, Jason P.; Kubala, Lukas
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation. Journal Article
In: Oxidative medicine and cellular longevity, vol. 2016, pp. 5219056, 2016, ISSN: 1942-0994 1942-0900, (Place: United States).
Abstract | Links | BibTeX | Tags: Acute Disease, Acute Lung Injury/complications/genetics, Animals, Inborn Errors/*complications, Inbred C57BL, Knockout, Leukocyte Disorders/*complications/*genetics, Lipopolysaccharides, Male, metabolism, Mice, Neutrophils/*pathology, Peroxidase/deficiency/genetics, Pneumonia/chemically induced/*complications/genetics
@article{kremserova_lung_2016,
title = {Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation.},
author = {Silvie Kremserova and Tomas Perecko and Karel Soucek and Anna Klinke and Stephan Baldus and Jason P. Eiserich and Lukas Kubala},
doi = {10.1155/2016/5219056},
issn = {1942-0994 1942-0900},
year = {2016},
date = {2016-01-01},
journal = {Oxidative medicine and cellular longevity},
volume = {2016},
pages = {5219056},
abstract = {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.},
note = {Place: United States},
keywords = {Acute Disease, Acute Lung Injury/complications/genetics, Animals, Inborn Errors/*complications, Inbred C57BL, Knockout, Leukocyte Disorders/*complications/*genetics, Lipopolysaccharides, Male, metabolism, Mice, Neutrophils/*pathology, Peroxidase/deficiency/genetics, Pneumonia/chemically induced/*complications/genetics},
pubstate = {published},
tppubtype = {article}
}
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.