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首页> 外文期刊>Applied Microbiology >A Toxic Environment: a Growing Understanding of How Microbial Communities Affect Escherichia coli O157:H7 Shiga Toxin Expression
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A Toxic Environment: a Growing Understanding of How Microbial Communities Affect Escherichia coli O157:H7 Shiga Toxin Expression

机译：有毒环境：对微生物社区如何影响大肠杆菌O157的越来越高兴：H7滋阴毒素表达

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Enterohemorrhagic Escherichia coli (EHEC) strains, including E. coli O157:H7, cause severe illness in humans due to the production of Shiga toxin (Stx) and other virulence factors. Because Stx is coregulated with lambdoid prophage induction, its expression is especially susceptible to environmental cues. Infections with Stx-producing E. coli can be difficult to model due to the wide range of disease outcomes: some infections are relatively mild, while others have serious complications. Probiotic organisms, members of the gut microbiome, and organic acids can depress Stx production, in many cases by inhibiting the growth of EHEC strains. On the other hand, the factors currently known to amplify Stx act via their effect on the stx -converting phage. Here, we characterize two interactive mechanisms that increase Stx production by O157:H7 strains: first, direct interactions with phage-susceptible E. coli , and second, indirect amplification by secreted factors. Infection of susceptible strains by the stx -converting phage can expand the Stx-producing population in a human or animal host, and phage infection has been shown to modulate virulence in vitro and in vivo . Acellular factors, particularly colicins and microcins, can kill O157:H7 cells but may also trigger Stx expression in the process. Colicins, microcins, and other bacteriocins have diverse cellular targets, and many such molecules remain uncharacterized. The identification of additional Stx-amplifying microbial interactions will improve our understanding of E. coli O157:H7 infections and help elucidate the intricate regulation of pathogenicity in EHEC strains.
机译：Enterohemorrhagic大肠杆菌（EHEC）菌株，包括大肠杆菌O157：H7，由于滋阴（STX）和其他毒力因子的产生，人类引起严重疾病。因为STX是用枝形前驱诱导的植物核心，所以其表达尤其易于环境线索。由于疾病结果广泛的疾病结果，难以模型难以模型的感染：一些感染是相对温和的，而其他感染具有严重的并发症。益生菌生物，肠道微生物组的成员和有机酸可以抑制STX生产，在许多情况下抑制EHEC菌株的生长。另一方面，目前已知的因素通过它们对STX - 混合物噬菌体的影响扩增STX。在这里，我们表征了两种互动机制，其通过O157：H7菌株增加STX生产：首先，与噬菌体易感大肠杆菌的直接相互作用，以及通过分泌因子的第二种，间接扩增。 STX转换噬菌体的感染易感菌株可以扩增人或动物宿主中的STX产生群体，并且已经显示噬菌体感染在体外和体内调节毒力。无细胞因子，特别是凝灰蛋白和微基因，可以杀死O157：H7细胞，但也可以在该过程中触发STX表达。凝灰蛋白，微基因和其他菌丝具有多种细胞靶标，许多这样的分子保持不表达。鉴定额外的STX扩增微生物相互作用将改善我们对大肠杆菌O157：H7感染的理解，并帮助阐明EHEC菌株中的致病性的复杂调节。

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