Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation

0471982 - BFÚ 2017 RIV US eng J - Článek v odborném periodiku
Kremserová, Silvie - Perečko, Tomáš - Souček, Karel - Klinke, A. - Baldus, S. - Eiserich, J.P. - Kubala, Lukáš
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation.
Oxidative Medicine and Cellular Longevity. Roč. 2016, Č. 2016 (2016), č. článku 5219056. ISSN 1942-0900. E-ISSN 1942-0994
Grant CEP: GA ČR GCP305/12/J038
Institucionální podpora: RVO:68081707
Klíčová slova: nitrotyrosine formation * airway inflammation * mouse neutrophils * apoptosis
Kód oboru RIV: BO - Biofyzika
Impakt faktor: 4.593, rok: 2016

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.
Trvalý link: http://hdl.handle.net/11104/0269341