Lehrstuhl Für Zellbiologie, Fachbereich Biologie, Universität Konstanz, 78457 Konstanz, Germany.
Lehrstuhl Für Zellbiologie, Fachbereich Biologie, Universität Konstanz, 78457 Konstanz, Germany; Konstanz Research School Chemical Biology, Universität Konstanz, 78457 Konstanz, Germany.
Cell Host Microbe. 2020 May 13;27(5):793-808.e5. doi: 10.1016/j.chom.2020.03.010. Epub 2020 Apr 13.
Several pathogens suppress exfoliation, a key defense of epithelia against microbial colonization. Common among these pathogens, exemplified by Neisseria gonorrhoeae, is their ability to bind carcinoembryonic antigen-related cell adhesion molecules (CEACAMs). Gonococcal CEACAM engagement triggers the expression of CD105, which is necessary to block epithelial exfoliation, whereas homotypic CEACAM-CEACAM interactions or antibody-mediated CEACAM clustering does not lead to CD105 expression. Here, we show that CEACAM-associated bacteria release nitric oxide (NO) during anaerobic respiration, and membrane-permeable NO initiates a eukaryotic signaling pathway involving soluble guanylate cyclase (sGC), protein kinase G, and the transcription factor CREB to upregulate CD105 expression. A murine vaginal infection model with N. gonorrhoeae reveals this metabolic cross communication allows bacterial suppression of epithelial exfoliation to facilitate mucosal colonization. Disrupting NO-initiated responses in host cells re-establishes epithelial exfoliation and inhibits mouse genital tract colonization by N. gonorrhoeae, suggesting a host-directed approach to prevent bacterial infections.
几种病原体抑制表皮脱落,这是上皮组织抵御微生物定植的关键防御机制。这些病原体的一个共同特征是能够结合癌胚抗原相关细胞粘附分子(CEACAMs),淋病奈瑟菌就是其中的典型代表。淋病奈瑟菌与 CEACAM 的结合会触发 CD105 的表达,这对于阻断上皮细胞脱落是必要的,而同种型 CEACAM-CEACAM 相互作用或抗体介导的 CEACAM 聚集不会导致 CD105 的表达。在这里,我们表明,CEACAM 相关细菌在厌氧呼吸过程中释放一氧化氮(NO),并且膜通透性的 NO 会启动涉及可溶性鸟苷酸环化酶(sGC)、蛋白激酶 G 和转录因子 CREB 的真核信号通路,从而上调 CD105 的表达。淋病奈瑟菌的小鼠阴道感染模型表明,这种代谢交叉通讯允许细菌抑制上皮细胞脱落,从而促进粘膜定植。破坏宿主细胞中由 NO 引发的反应会重新建立上皮细胞脱落,并抑制淋病奈瑟菌对小鼠生殖道的定植,这表明可以采取宿主定向的方法来预防细菌感染。