Dysregulated gut microbiota is one of major pathogenic factors in the development of colitis. Dock2 acts as a guanine nucleotide exchange factor (GEF) and activates small G protein RAC1. Our previous study showed that, compared to wild type (WT) mice, Dock2−/− mice were more susceptible to colitis induced by Citrobacter rodentium infection. However, it is not clear whether gut microbiota affects the host susceptibility to enteric bacterial infection in Dock2−/− mice. In this study, we demonstrated that Dock2 regulated the gut microbiota and affected the host susceptibility to C. rodentium infection by co-housing, fecal microbiota transfer and antibiotic treatment methods. Microbiota analysis by 16 S rRNA gene sequencing showed that Dock2 increased the abundance of prevotellaceae-NK3B31-group and Lactobacillus but decreased that of Helicobacter. These results suggest that Dock2 regulates the composition of gut microbiota and affects the host susceptibility to C. rodentium infection.

中文翻译：

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Dock2通过调节肠道微生物群影响宿主对柠檬酸杆菌感染的易感性

肠道菌群失调是结肠炎发展的主要致病因素之一。Dock2 充当鸟嘌呤核苷酸交换因子 (GEF) 并激活小 G 蛋白 RAC1。我们之前的研究表明，与野生型 (WT) 小鼠相比，Dock2-/- 小鼠更容易受到柠檬酸杆菌感染引起的结肠炎的影响。然而，尚不清楚肠道微生物群是否会影响宿主对 Dock2-/- 小鼠肠道细菌感染的易感性。在这项研究中，我们证明了 Dock2 通过共舍、粪便微生物群转移和抗生素治疗方法调节肠道微生物群并影响宿主对 C.rodentium 感染的易感性。通过 16 S rRNA 基因测序的微生物群分析表明，Dock2 增加了前藻科-NK3B31-group 和乳酸杆菌的丰度，但降低了螺杆菌的丰度。