Non-pathogenic Escherichia coli Enhance Stx2a Production of E. coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms.
Non-pathogenic Escherichia coli Enhance Stx2a Production of E. coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms.
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DOI：
10.3389/fmicb.2018.01325
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发表时间：
2018
影响因子：
5.2
通讯作者：
Dudley EG
中科院分区：
文献类型：
--
作者：
Xiaoli L;Figler HM;Goswami Banerjee K;Hayes CS;Dudley EG
由食源性致病菌O157：H7引起的肠道定植会导致严重的疾病症状，包括溶血性尿毒症综合征(HUS)和出血性结肠炎(HC)。一种或多种志贺毒素(STX)的合成对HUS和HC的发展至关重要。编码STX的基因，包括Stx2a，是在整合在E.ColiO157：H7染色体上的Lambdoid原噬菌体中发现的。当特定的非致病性大肠杆菌菌株与O157：H7共培养时，Stx2a的表达增强，推测这种表型要求非致病性大肠杆菌对STX转化噬菌体感染敏感。我们通过产生抗噬菌体的非致病性大肠杆菌菌株来检验这一假设，其中BAMA(一个必要的基因和STX噬菌体受体)被来自其他物种的同源基因替换。这种异源基因替换使实验室菌株E.coliC600与属于超强毒力第8分支的E.ColiO157：H7菌株PA2共培养时不能提高毒素产生的能力。BAMA的胞外环(环4、6、7)进一步表明，在STx2a转化噬菌体的感染过程中，胞外环是重要的。然而，在另一种命名为1.1954的共生大肠杆菌中，类似的基因替换揭示了一种不依赖于巴马的毒素放大机制。毒素增加1.1954不是通过另一种受体(羔羊或FADL)感染噬菌体的结果，也不是通过转化stx2a噬菌体形成溶原体的结果，也不是分泌分子的产生。总而言之，这些数据表明，非致病性大肠杆菌可以通过至少两种机制促进毒素的产生。
Intestinal colonization by the foodborne pathogen Escherichia coli O157:H7 leads to serious disease symptoms, including hemolytic uremic syndrome (HUS) and hemorrhagic colitis (HC). Synthesis of one or more Shiga toxins (Stx) is essential for HUS and HC development. The genes encoding Stx, including Stx2a, are found within a lambdoid prophage integrated in the E. coli O157:H7 chromosome. Enhanced Stx2a expression was reported when specific non-pathogenic E. coli strains were co-cultured with E. coli O157:H7, and it was hypothesized that this phenotype required the non-pathogenic E. coli to be sensitive to stx-converting phage infection. We tested this hypothesis by generating phage resistant non-pathogenic E. coli strains where bamA (an essential gene and Stx phage receptor) was replaced with an ortholog from other species. Such heterologous gene replacement abolished the ability of the laboratory strain E. coli C600 to enhance toxin production when co-cultured with E. coli O157:H7 strain PA2, which belongs to the hypervirulent clade 8. The extracellular loops of BamA (loop 4, 6, 7) were further shown to be important for infection by stx2a-converting phages. However, similar gene replacement in another commensal E. coli, designated 1.1954, revealed a bamA-independent mechanism for toxin amplification. Toxin enhancement by 1.1954 was not the result of phage infection through an alternative receptor (LamB or FadL), lysogen formation by stx2a-converting phages, or the production of a secreted molecule. Collectively, these data suggest that non-pathogenic E. coli can enhance toxin production through at least two mechanisms.