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.

中文翻译：

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有毒的环境：人们越来越了解微生物群落如何通过大肠杆菌O157：H7影响志贺毒素的表达。

肠出血性大肠杆菌（EHEC）菌株，包括大肠杆菌O157：H7，由于产生志贺毒素（Stx）和其他毒力因子而在人类中引起严重疾病。由于Stx与lambdoid噬菌体诱导共调节，因此其表达特别容易受到环境提示的影响。由于疾病的结果范围广泛，可能难以模拟产生Stx的大肠杆菌的感染：某些感染相对较轻，而另一些则具有严重的并发症。益生菌，肠道微生物组成员和有机酸可在许多情况下通过抑制EHEC菌株的生长来抑制Stx的产生。在另一方面，目前的因素通过其对影响知扩增的Stx行为STX-转化噬菌体。在这里，我们表征了两种相互作用的机制，它们通过O157：H7菌株增加Stx的产生：第一，与噬菌体易感性大肠杆菌的直接相互作用，第二，由分泌因子的间接扩增。由敏感菌株的感染STX -转化噬菌体可扩大在人类或动物宿主中产STX人口和噬菌体感染已显示可调节的毒力在体外和体内。非细胞因子，特别是大肠菌素和微素，可以杀死O157：H7细胞，但也可能在此过程中触发Stx表达。大肠菌素，微素和其他细菌素具有多种细胞靶标，许多此类分子仍未鉴定。鉴定其他增强Stx的微生物相互作用将增进我们对大肠杆菌O157：H7感染的了解，并有助于阐明EHEC菌株致病性的复杂调控。