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首页> 外文期刊>Journal of bacteriology >FdhTU-Modulated Formate Dehydrogenase Expression and Electron Donor Availability Enhance Recovery of Campylobacter jejuni following Host Cell Infection
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FdhTU-Modulated Formate Dehydrogenase Expression and Electron Donor Availability Enhance Recovery of Campylobacter jejuni following Host Cell Infection

机译：FdhTU调制的甲酰胺脱氢酶表达和电子供体可用性增强宿主细胞感染后空肠弯曲杆菌的恢复

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Campylobacter jejuni is a food-borne bacterial pathogen that colonizes the intestinal tract and causes severe gastroenteritis. Interaction with host epithelial cells is thought to enhance severity of disease, and the ability of C. jejuni to modulate its metabolism in different in vivo and environmental niches contributes to its success as a pathogen. A C. jejuni operon comprising two genes that we designated fdhT (CJJ81176_1492) and fdhU (CJJ81176_1493) is conserved in many bacterial species. Deletion of fdhT or fdhU in C. jejuni resulted in apparent defects in adherence and/or invasion of Caco-2 epithelial cells when assessed by CFU enumeration on standard Mueller-Hinton agar. However, fluorescence microscopy indicated that each mutant invaded cells at wild-type levels, instead suggesting roles for FdhTU in either intracellular survival or postinvasion recovery. The loss of fdhU caused reduced mRNA levels of formate dehydrogenase (FDH) genes and a severe defect in FDH activity. Cell infection phenotypes of a mutant deleted for the FdhA subunit of FDH and an ΔfdhU ΔfdhA double mutant were similar to those of a ΔfdhU mutant, which likewise suggested that FdhU and FdhA function in the same pathway. Cell infection assays followed by CFU enumeration on plates supplemented with sodium sulfite abolished the ΔfdhU and ΔfdhA mutant defects and resulted in significantly enhanced recovery of all strains, including wild type, at the invasion and intracellular survival time points. Collectively, our data indicate that FdhTU and FDH are required for optimal recovery following cell infection and suggest that C. jejuni alters its metabolic potential in the intracellular environment.
机译：空肠弯曲杆菌是一种食源性细菌病原体，可在肠道内定植并引起严重的肠胃炎。与宿主上皮细胞的相互作用被认为可增强疾病的严重性和 C的能力。空肠在不同的体内调节其新陈代谢，环境小生境有助于空肠作为病原体的成功。 C。空肠操纵子包含两个我们称为 fdhT （ CJJ81176_1492 ）和 fdhU （ CJJ81176_1493 ）的基因在许多细菌物种中都是保守的。在 C中删除 fdhT 或 fdhU 。通过在标准Mueller-Hinton琼脂上进行CFU枚举评估，空肠对Caco-2上皮细胞的粘附和/或侵袭产生明显的缺陷。然而，荧光显微镜显示每个突变体都以野生型水平侵袭细胞，相反提示FdhTU在细胞内存活或侵袭后恢复中的作用。 fdhU 的丧失导致甲酸脱氢酶（FDH）基因的mRNA水平降低，以及FDH活性严重缺陷。 FDH FdhA亚基缺失的突变体和Δ fdhU Δ fdhA 双突变体的细胞感染表型与Δ fdhU 相似突变体，同样提示FdhU和FdhA在同一途径中起作用。细胞感染分析，然后在补充亚硫酸钠的平板上进行CFU计数，消除了Δ fdhU 和Δ fdhA 突变体缺陷，并显着提高了所有菌株的回收率，包括野生型，在侵袭和细胞内存活时间点。总的来说，我们的数据表明FdhTU和FDH是细胞感染后最佳恢复所必需的，并提示 C。空肠在细胞内环境中会改变其代谢潜能。

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