Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Marchioninistraße 17, 81377 München, Germany.
Int J Med Microbiol. 2010 Nov;300(7):429-34. doi: 10.1016/j.ijmm.2010.02.006. Epub 2010 May 23.
Extraintestinal pathogenic Escherichia coli (ExPECs) possess an armament of virulence factors to colonize and infect the host, such as adhesins, toxins, capsules and iron-uptake systems. Recently, we could identify a novel virulence factor of ExPECs that interferes with the innate immune response of the host by interrupting the NF-κB signaling pathway. This protein named TcpC shows considerable homology to motifs of the Tir domain of Toll-like receptors. Here we demonstrate that the tcpC gene is widely distributed among clinical ExPEC isolates with almost half of the E. coli strains from patients suffering pyelonephritis shown to be tcpC positive as compared to only 8% in commensal isolates. However, this gene is only present in phylogenetic group B2 strains. Interestingly, the tcpC gene is strongly associated with presence of the high-pathogenicity island (HPI). The phylogenetic history of the tcpC gene, in the E. coli reference collection (ECOR) and other well-defined E. coli strains, compared to the phylogenetic histories of the HPI and the strains, showed that the tcpC gene (i) is scattered among various B2 subgroups with specific O-types, (ii) has a phylogeny incongruent with the strain phylogeny, but (iii) congruent with the HPI phylogenetic history. This, together with the strong conservation of the tcpC gene, indicates a very recent introduction of this virulence factor into E. coli by horizontal gene transfer which occurred "en bloc" with the HPI at one major hot spot of recombination in the E. coli genome. The present data provide evidence for a strong impact of homologous recombination events in the spread of the TcpC virulence trait among E. coli.
肠外致病性大肠杆菌（ExPECs）拥有一套毒力因子，用于定植和感染宿主，如黏附素、毒素、荚膜和铁摄取系统。最近，我们发现了一种 ExPEC 的新毒力因子，它通过中断 NF-κB 信号通路来干扰宿主的固有免疫反应。这种名为 TcpC 的蛋白质与 Toll 样受体 Tir 结构域的基序具有相当大的同源性。在这里，我们证明 tcpC 基因在临床 ExPEC 分离株中广泛分布，几乎一半来自肾盂肾炎患者的大肠杆菌菌株呈 tcpC 阳性，而共生分离株中只有 8%呈阳性。然而，该基因仅存在于进化群 B2 菌株中。有趣的是，tcpC 基因与高致病性岛（HPI）的存在密切相关。在大肠杆菌参考集（ECOR）和其他明确定义的大肠杆菌菌株中，tcpC 基因的进化历史与 HPI 和菌株的进化历史相比，表明 tcpC 基因 (i) 分散在具有特定 O 型的各种 B2 亚群中，(ii) 与菌株进化历史不一致，但 (iii) 与 HPI 进化历史一致。这与 tcpC 基因的强烈保守性一起表明，这种毒力因子是通过水平基因转移最近才被引入大肠杆菌的，它与 HPI 一起在大肠杆菌基因组的一个主要重组热点上“整块”转移。这些数据为同源重组事件在 TcpC 毒力特性在大肠杆菌中的传播中产生的强烈影响提供了证据。
