Citrobacter Infection and Wnt signaling.
Citrobacter Infection and Wnt signaling.
复制标题
柠檬酸杆菌感染和Wnt信号传导。
DOI：
10.1007/s11888-012-0143-4
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发表时间：
2012-12
影响因子：
--
通讯作者：
Umar, Shahid
中科院分区：
文献类型：
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作者：
Umar, Shahid
肠道植物群通常有助于健康的环境，而影响先天性和适应性免疫应答的肠道和病原性细菌两者都可以引起急性和/或慢性粘膜炎症。啮齿类柠檬酸杆菌（Citrobacter rodentium，C.啮齿动物）是肠道病原体家族的成员，其提供了极好的体内模型以实时研究宿主-病原体相互作用。它是小鼠传染性结肠增生（transmissible murine colonic hyperplasia，TMCH）的病原体，而C.啮齿类感染取决于遗传背景。迄今为止，在该模型中正在进行和已完成的研究已经确定，Wnt/β-连环蛋白、Notch和PI 3 K途径调节结肠隐窝增生，而由MEK/ERK/NF-κB信号传导介导的上皮-基质串扰调节易感品系中的炎症和/或结肠炎。梭啮齿类动物诱导的增生状态也增加了对诱变损伤或Apc基因杂合子小鼠的易感性。调节宿主对C.因此，啮齿动物感染提供了一个机会，以描绘机制，确定粘膜增生，肠道炎症，和/或肿瘤的疾病结果。
Gut flora generally contributes to a healthy environment while both commensal and pathogenic bacteria that influence the innate and adaptive immune responses, can cause acute and/or chronic mucosal inflammation. Citrobacter rodentium (C. rodentium) is a member of the family of enteropathogens that provide an excellent in vivo model to investigate the host-pathogen interactions in real-time. It is the etiologic agent for transmissible murine colonic hyperplasia (TMCH) while inflammation following C. rodentium infection is dependent upon the genetic background. Ongoing and completed studies in this model have so far established that Wnt/β-catenin, Notch and PI3K pathways regulate colonic crypt hyperplasia while epithelial-stromal cross-talk, mediated by MEK/ERK/NF-κB signaling, regulates inflammation and/or colitis in susceptible strains. The C. rodentium-induced hyperplastic state also increases the susceptibility to either mutagenic insult or in mice heterozygous for Apc gene. The ability to modulate the host response to C. rodentium infection therefore provides an opportunity to delineate the mechanisms that determine mucosal hyperplasia, intestinal inflammation, and/or neoplasia as disease outcomes.