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首页> 外文期刊>Applied Microbiology >Differential Induction of Antimicrobial REGIII by the Intestinal Microbiota and Bifidobacterium breve NCC2950
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Differential Induction of Antimicrobial REGIII by the Intestinal Microbiota and Bifidobacterium breve NCC2950

机译：肠道菌群和短双歧杆菌NCC2950对抗生素REGIII的差异诱导

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The intestinal microbiota is a key determinant of gut homeostasis, which is achieved, in part, through regulation of antimicrobial peptide secretion. The aim of this study was to determine the efficiency by which members of the intestinal microbiota induce the antimicrobial peptide REGIII and to elucidate the underlying pathways. We showed that germfree mice have low levels of REGIII-γ in their ileum and colon compared to mice with different intestinal microbiota backgrounds. Colonization with a microbiota of low diversity (altered Schaedler flora) did not induce the expression of REGIII-γ as effectively as a complex community (specific pathogen free). Monocolonization with the probiotic Bifidobacterium breve , but not with the nonprobiotic commensal Escherichia coli JM83, upregulated REGIII-γ expression. Induction of REGIII-γ by B. breve was abrogated in mice lacking MyD88 and Ticam1 signaling. Both live and heat-inactivated B. breve but not spent culture medium from B. breve induced the expression of REGIII-α, the human ortholog and homolog of REGIII-γ, in human colonic epithelial cells (Caco-2). Taken together, the results suggest that REGIII-γ expression in the intestine correlates with the richness of microbiota composition. Also, specific bacteria such as Bifidobacterium breve NCC2950 effectively induce REGIII production in the intestine via the MyD88-Ticam1 pathway. Treatment with this probiotic may enhance the mucosal barrier and protect the host from infection and inflammation.
机译：肠道菌群是肠道稳态的关键决定因素，这部分通过调节抗菌肽的分泌来实现。这项研究的目的是确定肠道菌群成员诱导抗菌肽REGIII的效率，并阐明其基本途径。我们显示，与具有不同肠道菌群背景的小鼠相比，无菌小鼠在回肠和结肠中的REGIII-γ水平较低。低多样性微生物群落（改变的舍德勒菌群）的定殖不能像复杂群落（不含特定病原体）一样有效地诱导REGIII-γ的表达。用益生菌短双歧杆菌进行单结肠化，但用非益生共生大肠杆菌JM83进行单克隆，上调REGIII-γ的表达。在缺乏MyD88和Ticam1信号转导的小鼠中，短双歧杆菌对REGIII-γ的诱导被废除。活的和热灭活的短双歧杆菌，但未用过的短双歧杆菌培养基在人结肠上皮细胞（Caco-2）中诱导REGIII-α（REGIII-γ的人直系同源物和同源物）的表达。两者合计，结果表明在肠中的REGIII-γ表达与微生物群组成的丰富性相关。此外，特定的细菌（如短双歧杆菌NCC2950）可通过MyD88-Ticam1途径在肠道中有效诱导REGIII的产生。用这种益生菌治疗可能会增强粘膜屏障并保护宿主免受感染和炎症。

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