Vibrio cholerae high cell density quorum sensing activates the host intestinal innate immune response.
Vibrio cholerae high cell density quorum sensing activates the host intestinal innate immune response.
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DOI：
10.1016/j.celrep.2022.111368
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发表时间：
2022-09-20
期刊：
影响因子：
8.8
通讯作者：
Watnick, Paula I.
中科院分区：
文献类型：
--
作者：
Jugder, Bat-Erdene;Batista, Juliana H.;Gibson, Jacob A.;Cunningham, Paul M.;Asara, John M.;Watnick, Paula I.
群体感应从根本上改变了霍乱弧菌与水生环境、环境宿主和人类肠道的相互作用。在高细胞密度下，群体感应调节因子 HapR 不仅抑制霍乱毒素和毒素共同调节的菌毛（人类感染中必需的毒力因子）的表达，而且抑制非生物和生物表面附着所需的弧菌多糖（VPS）胞外多糖基质的合成。在这里，我们描述了霍乱弧菌群体感应的一个特征，该特征将宿主与病原体的相互作用转向共生。通过抑制病原体消耗性合成代谢，特别是色氨酸的摄取，霍乱弧菌 HapR 刺激宿主肠道血清素的产生。这反过来又激活宿主肠道先天免疫信号以促进宿主生存。在这里，贾格德等人。表明霍乱弧菌掌握高细胞密度调节因子 HapR 抑制病原体色氨酸消耗。这为宿主肠细胞提供了血清素合成的前体，从而激活肠道先天免疫信号并延长宿主的生存。因此，霍乱弧菌 HapR 促进与宿主的共生关系。
Quorum sensing fundamentally alters the interaction of Vibrio cholerae with aquatic environments, environmental hosts, and the human intestine. At high cell density, the quorum-sensing regulator HapR represses not only expression of cholera toxin and the toxin co-regulated pilus, virulence factors essential in human infection, but also synthesis of the Vibrio polysaccharide (VPS) exopolysaccharide-based matrix required for abiotic and biotic surface attachment. Here, we describe a feature of V. cholerae quorum sensing that shifts the host-pathogen interaction toward commensalism. By repressing pathogen consumptive anabolic metabolism and, in particular, tryptophan uptake, V. cholerae HapR stimulates host intestinal serotonin production. This, in turn, activates host intestinal innate immune signaling to promote host survival. Here, Jugder et al. show that the V. cholerae master high cell density regulator HapR represses pathogen tryptophan consumption. This provides host enterocytes precursors for serotonin synthesis, which activates intestinal innate immune signaling and prolongs host survival. Thus, V. cholerae HapR promotes a commensal relationship with the host.
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