Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation.
Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation.
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DOI：
10.1155/2016/5219056
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发表时间：
2016
影响因子：
--
通讯作者：
Kubala L
中科院分区：
文献类型：
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作者：
Kremserova S;Perecko T;Soucek K;Klinke A;Baldus S;Eiserich JP;Kubala L
全身性炎症伴随疾病，如败血症，主要影响肺，并诱导其衰竭。这仍然是脓毒症诱导死亡的最常见原因。虽然中性粒细胞在肺衰竭中起关键作用，但其机制仍不完全。我们报告髓过氧化物酶（MPO），在中性粒细胞颗粒丰富的酶，调节急性肺部炎症反应的过程中所引起的鼻内应用脂多糖。MPO缺陷型小鼠在整个肺部炎症过程中气道浸润的中性粒细胞数量显著增加。这伴随着MPO缺陷小鼠支气管肺泡灌洗液中RANTES水平升高。肺损伤和炎症的其他标志物，这有助于招募中性粒细胞进入发炎的肺，包括总蛋白和其他选定的促炎细胞因子没有显着不同的支气管肺泡灌洗液从野生型和MPO缺陷型小鼠。有趣的是，MPO缺陷的中性粒细胞显示出以磷脂酰丝氨酸表面表达为特征的细胞死亡率降低。总的来说，MPO在调节肺部炎症中的重要性，独立于其假定的杀微生物功能，可能与MPO调节中性粒细胞寿命和影响炎症部位趋化因子积累的能力有关。
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 wild-type 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.