Fitzhenry R J, Reece S, Trabulsi L R, Heuschkel R, Murch S, Thomson M, Frankel G, Phillips A D
Centre for Paediatric Gastroenterology, Royal Free Hospital and University College Medical School, London, United Kingdom.
Infect Immun. 2002 Aug;70(8):4362-8. doi: 10.1128/IAI.70.8.4362-4368.2002.
Four enteropathogenic Escherichia coli (EPEC) strains belonging to the O55 serogroup (G21 and G30 [both O55:H6], G35 [O55:H-], and G58 [O55:H7]) were tested for their tissue tropism by using human intestinal in vitro organ culture. Strains showed restricted adhesion with attaching-and-effacing activity to follicle-associated epithelium of Peyer's patches, with no apparent adhesion to duodenum or colon. G35 and G58 express intimin gamma and show a similar tropism to intimin gamma-expressing enterohemorrhagic E. coli (EHEC) O157:H7. However, strains G21 and G30 were unusual because they expressed intimin alpha and had a restricted tissue tropism of intimin gamma phenotype. The amino acid sequence of the carboxy-terminal 280 amino acids of intimin from G21 was determined. Comparison with the prototype intimin alpha from strain E2348/69 (O127:H6) showed a single amino acid difference (corresponding to Val907 and Ala907 in the whole intimins). This mutation was reproduced by site-directed mutagenesis in an intimin alpha plasmid template, pCVD438, with the hypothesis that it may induce a change in tropism. However, when the mutated plasmid was placed in both EPEC and EHEC backgrounds, duodenal adhesion in a manner similar to strain E2348/69 was evident upon in vitro organ culture. Thus, additional factor(s) unrelated to intimin exist in the O55:H6 genome that influence human intestinal tissue tropism.
利用人肠道体外器官培养,对4株属于O55血清群的肠致病性大肠杆菌(EPEC)菌株(G21和G30 [均为O55:H6]、G35 [O55:H -]和G58 [O55:H7])进行了组织嗜性测试。这些菌株表现出有限的黏附,并对派尔集合淋巴结的滤泡相关上皮具有紧密黏附并抹除微绒毛的活性,对十二指肠或结肠无明显黏附。G35和G58表达γ- intimin,并表现出与表达γ- intimin的肠出血性大肠杆菌(EHEC)O157:H7相似的嗜性。然而,G21和G30菌株不同寻常,因为它们表达α- intimin,且具有γ- intimin表型的有限组织嗜性。测定了G21菌株intimin羧基末端280个氨基酸的序列。与来自菌株E2348/69(O127:H6)的α- intimin原型相比,发现有一个氨基酸差异(在整个intimin中对应于Val907和Ala907)。通过定点诱变在intiminα质粒模板pCVD438中重现了这种突变,推测它可能导致嗜性改变。然而,当将突变质粒置于EPEC和EHEC背景中时,体外器官培养显示其以类似于菌株E2348/69的方式黏附于十二指肠。因此,O55:H6基因组中存在与intimin无关的其他因素影响人肠道组织嗜性。