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首页> 外文期刊>Innate immunity >IL-17A attracts inflammatory cells in murine lung infection with P-aeruginosa
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IL-17A attracts inflammatory cells in murine lung infection with P-aeruginosa

机译:IL-17A吸引小鼠肺部感染P-铜绿假单胞菌的炎症细胞

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摘要

IL-17A-dependent immunity is of importance in the protection against extracellular bacterial pathogens. However, IL-17A is also suggested to mediate the pathogenesis of lung diseases, such as acute respiratory distress syndrome. Here, we studied the role of IL-17A in a mouse model of acute pneumonia. IL-17A mediated the expression of keratinocyte-derived chemokine (KC) and the recruitment of inflammatory cells in mice infected with a sub-lethal dose of Pseudomonas aeruginosa. IL-17A deficiency protected mice from lethal P.aeruginosa lung infection. A sub-lethal infection with Streptococcus pneumoniae resulted in increased bacterial burden associated with increased pulmonary inflammation. Thus, the type of infectious bacteria seemed to influence the way in which IL-17A functions during pulmonary infection. Reducing pulmonary inflammation by targeting IL-17A may be a therapeutic option in acute P. aeruginosa pneumonia.
机译:IL-17A依赖性免疫对细胞外细菌病原体的保护具有重要意义。然而,IL-17A也被建议介导诸如急性呼吸窘迫综合征等肺部疾病的发病机制。在这里,我们研究了IL-17A在急性肺炎小鼠模型中的作用。 IL-17A介导了在致死剂量的铜绿假单胞菌感染的小鼠中角质形成细胞趋化因子(KC)的表达和炎症细胞的募集。 IL-17A缺乏症可保护小鼠免受致命的铜绿假单胞菌肺部感染。肺炎链球菌的亚致死性感染导致细菌负担增加,并伴有肺部炎症增加。因此,传染性细菌的类型似乎影响了IL-17A在肺部感染过程中的功能方式。通过靶向IL-17A减轻肺部炎症可能是急性铜绿假单胞菌肺炎的治疗选择。

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