CD36 Provides Host Protection Against Klebsiella pneumoniae Intrapulmonary Infection by Enhancing Lipopolysaccharide Responsiveness and Macrophage Phagocytosis
CD36 Provides Host Protection Against Klebsiella pneumoniae Intrapulmonary Infection by Enhancing Lipopolysaccharide Responsiveness and Macrophage Phagocytosis
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DOI：
10.1093/infdis/jiw451
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发表时间：
2016-12-15
影响因子：
6.4
通讯作者：
Lee, Janet S.
中科院分区：
文献类型：
--
作者：
Olonisakin, Tolani F.;Li, Huihua;Lee, Janet S.
肺炎克雷伯氏菌仍然是世界范围内肺内感染和侵袭性疾病的重要原因。K.肺炎克雷伯氏菌主要通过表达多糖荚膜来逃避血清杀伤和吞噬作用，但其致病性也受宿主因素的影响。我们研究了识别病原体和修饰的自身配体的清道夫受体CD36是否是K.肺炎病原性。尽管3种不同克雷伯氏菌的血清敏感性和毒力存在差异。pneumoniae（高粘滞性K1、研究K2和产碳青霉烯酶的ST 258）菌株中，CD36的缺失显著增加宿主对肺炎克雷伯氏菌急性肺内感染的易感性。肺炎，无论菌株如何。我们证明CD36增强LPS对K.肺炎球菌的细胞因子产生和巨噬细胞吞噬作用，其不依赖于多糖荚膜抗原。我们的研究为K的宿主决定因素提供了新的见解。pneumoniae的致病性，并提出了CD36的功能突变可能使个体易患克雷伯氏菌的可能性。肺炎综合征
Klebsiella pneumoniae remains an important cause of intrapulmonary infection and invasive disease worldwide. K. pneumoniae can evade serum killing and phagocytosis primarily through the expression of a polysaccharide capsule, but its pathogenicity is also influenced by host factors. We examined whether CD36, a scavenger receptor that recognizes pathogen and modified self ligands, is a host determinant of K. pneumoniae pathogenicity. Despite differences in serum sensitivity and virulence of 3 distinct K. pneumoniae (hypermucoviscous K1, research K2, and carbapenemase-producing ST258) strains, the absence of CD36 significantly increased host susceptibility to acute intrapulmonary infection by K. pneumoniae, regardless of strain. We demonstrate that CD36 enhances LPS responsiveness to K. pneumoniae to increase downstream cytokine production and macrophage phagocytosis that is independent of polysaccharide capsular antigen. Our study provides new insights into host determinants of K. pneumoniae pathogenicity and raises the possibility that functional mutations in CD36 may predispose individuals to K. pneumoniae syndromes.