J 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

Štítky

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.