Detailed Information on Publication Record
2016
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation
KREMSEROVÁ, Silvie, Tomáš PEREČKO, Karel SOUČEK, A. KLINKE, S. BALDUS et. al.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
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10601 Cell biology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 4.593
RIV identification code
RIV/00216224:14310/16:00100431
Organization unit
Faculty of Science
UT WoS
000374867600001
Keywords in English
NITROTYROSINE FORMATION; AIRWAY INFLAMMATION; MOUSE NEUTROPHILS; APOPTOSIS; ACTIVATION; ACID; RESOLUTION; IMMUNITY; DISEASE; INJURY
Tags
International impact, Reviewed
Změněno: 13/4/2018 14:22, Ing. Nicole Zrilić
Abstract
V originále
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.