Department of Microbiology and Immunology, Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, Buffalo, New York, USA.
Mucosal Immunol. 2010 May;3(3):312-21. doi: 10.1038/mi.2009.139. Epub 2010 Jan 27.
Host immune responses, including the characteristic influx of neutrophils, against Neisseria gonorrhoeae are poorly understood; adaptive immunity is minimal and non-protective. We hypothesize that N. gonorrhoeae selectively elicits Th17-dependent responses, which trigger innate defense mechanisms, including neutrophils and antimicrobial proteins, that it can resist. We found that N. gonorrhoeae induced the production of interleukin-17 (IL-17) in mouse T-cells and Th17-inducing cytokines in mouse and human APCs in vitro. IL-17 was induced in the iliac lymph nodes in vivo in a female mouse model of genital tract gonococcal infection. Antibody blockade of IL-17 or deletion of the major IL-17 receptor (IL-17R) in IL-17RA(KO) mice led to prolonged infection and diminished neutrophil influx. Genital tract tissue from IL-17RA(KO) mice showed reduced production of neutrophil-attractant chemokines in response to culture with N. gonorrhoeae. These results imply a crucial role for IL-17 and Th17 cells in the immune response to N. gonorrhoeae.
宿主的免疫反应，包括中性粒细胞的特征性涌入，对淋病奈瑟菌的了解甚少；适应性免疫是最小的，没有保护作用。我们假设淋病奈瑟菌选择性地引发了 Th17 依赖性反应，这些反应触发了先天防御机制，包括中性粒细胞和抗菌蛋白，而淋病奈瑟菌可以抵抗这些机制。我们发现，淋病奈瑟菌在体外诱导了小鼠 T 细胞产生白细胞介素-17（IL-17）和 Th17 诱导细胞因子，并在体内雌性小鼠生殖道淋病奈瑟菌感染模型中诱导了 IL-17 在髂淋巴结中的产生。IL-17 的产生在白细胞介素-17 受体（IL-17R）缺陷型（IL-17RA（KO））小鼠中导致感染延长和中性粒细胞涌入减少。IL-17RA（KO）小鼠生殖道组织对淋病奈瑟菌培养的反应中，中性粒细胞趋化因子的产生减少。这些结果表明，IL-17 和 Th17 细胞在针对淋病奈瑟菌的免疫反应中起着至关重要的作用。
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