KREMSEROVÁ, Silvie, Tomáš PEREČKO, Karel SOUČEK, A. KLINKE, S. BALDUS, J.P. EISERICH and Lukáš KUBALA. Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation. Oxidative Medicine and Cellular Longevity. London: HINDAWI LTD, 2016, vol. 2016, No 1, p. nestránkováno, 13 pp. ISSN 1942-0900. Available from: https://dx.doi.org/10.1155/2016/5219056.
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Basic information
Original name Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation
Authors KREMSEROVÁ, Silvie (203 Czech Republic, belonging to the institution), Tomáš PEREČKO (703 Slovakia, belonging to the institution), Karel SOUČEK (203 Czech Republic, belonging to the institution), A. KLINKE (276 Germany), S. BALDUS (276 Germany), J.P. EISERICH (840 United States of America) and Lukáš KUBALA (203 Czech Republic, guarantor, belonging to the institution).
Edition Oxidative Medicine and Cellular Longevity, London, HINDAWI LTD, 2016, 1942-0900.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 4.593
RIV identification code RIV/00216224:14310/16:00100431
Organization unit Faculty of Science
Doi http://dx.doi.org/10.1155/2016/5219056
UT WoS 000374867600001
Keywords in English NITROTYROSINE FORMATION; AIRWAY INFLAMMATION; MOUSE NEUTROPHILS; APOPTOSIS; ACTIVATION; ACID; RESOLUTION; IMMUNITY; DISEASE; INJURY
Tags NZ, rivok
Tags International impact, Reviewed
Changed by Changed by: Ing. Nicole Zrilić, učo 240776. Changed: 13/4/2018 14:22.
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 wildtype 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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