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.Základní údaje
Originální název
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation
Autoři
KREMSEROVÁ, Silvie (203 Česká republika, domácí), Tomáš PEREČKO (703 Slovensko, domácí), Karel SOUČEK (203 Česká republika, domácí), A. KLINKE (276 Německo), S. BALDUS (276 Německo), J.P. EISERICH (840 Spojené státy) a Lukáš KUBALA (203 Česká republika, garant, domácí)
Vydání
Oxidative Medicine and Cellular Longevity, London, HINDAWI LTD, 2016, 1942-0900
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
10601 Cell biology
Stát vydavatele
Velká Británie a Severní Irsko
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 4.593
Kód RIV
RIV/00216224:14310/16:00100431
Organizační jednotka
Přírodovědecká fakulta
UT WoS
000374867600001
Klíčová slova anglicky
NITROTYROSINE FORMATION; AIRWAY INFLAMMATION; MOUSE NEUTROPHILS; APOPTOSIS; ACTIVATION; ACID; RESOLUTION; IMMUNITY; DISEASE; INJURY
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 13. 4. 2018 14:22, Ing. Nicole Zrilić
Anotace
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.