Miller V L, Farmer J J, Hill W E, Falkow S
Department of Medical Microbiology, Stanford University, California 94305.
Infect Immun. 1989 Jan;57(1):121-31. doi: 10.1128/iai.57.1.121-131.1989.
Yersinia enterocolitica is a heterogeneous group of organisms with more than 50 serotypes and several biotypes. Only a few of these serotypes cause gastrointestinal disease in otherwise healthy hosts; these serotypes are the pathogenic serotypes. Although Y. enterocolitica requires a high-molecular-weight plasmid to cause disease, chromosome-encoded determinants are required for the full expression of virulence. The ability of Yersinia spp. to invade eucaryotic cells is thought to be a virulence factor, because nonpathogenic serotypes are noninvasive in animals and in tissue culture cell models. Current evidence indicates that invasion ability is chromosome encoded. We recently reported cloning two loci, inv and ail, from Y. enterocolitica O8 strain 8081c that allow Escherichia coli to invade tissue culture cells. We investigated the link between invasion in an in vitro tissue culture invasion (TCI) model and hybridization to probes derived from the two invasion loci, inv and ail. We examined 177 Yersinia strains. Strains of serotypes and species associated with disease were TCI+, whereas strains of serotypes and species not associated with disease were TCI-. Only TCI+ strains had DNA homologous to probes derived from ail. All strains (TCI+ and TCI-) had DNA homologous to probes derived from inv, but there were certain restriction fragment-linked polymorphisms that were associated primarily with TCI+ strains. These observations held true for strains epidemiologically associated with disease. Both the inv and ail loci were found to be clearly located on the chromosome. No other genera, including other invasive organisms, had DNA homologous to inv or ail. These data support the hypothesis that the ail locus encodes a Y. enterocolitica invasion factor that may be involved in pathogenesis.
小肠结肠炎耶尔森菌是一组异质性微生物,有50多种血清型和几种生物型。其中只有少数血清型能在原本健康的宿主中引起胃肠道疾病;这些血清型就是致病血清型。虽然小肠结肠炎耶尔森菌引起疾病需要一个高分子量质粒,但毒力的充分表达还需要染色体编码的决定因素。耶尔森菌属侵入真核细胞的能力被认为是一种毒力因子,因为非致病血清型在动物和组织培养细胞模型中不具有侵袭性。目前的证据表明,侵袭能力是由染色体编码的。我们最近报道了从小肠结肠炎耶尔森菌O8菌株8081c中克隆出两个基因座,即inv和ail,它们能使大肠杆菌侵入组织培养细胞。我们研究了体外组织培养侵袭(TCI)模型中的侵袭与源自inv和ail这两个侵袭基因座的探针杂交之间的联系。我们检测了177株耶尔森菌菌株。与疾病相关的血清型和菌种的菌株是TCI阳性,而与疾病无关的血清型和菌种的菌株是TCI阴性。只有TCI阳性菌株具有与源自ail的探针同源的DNA。所有菌株(TCI阳性和TCI阴性)都具有与源自inv的探针同源的DNA,但存在某些主要与TCI阳性菌株相关的限制性片段连锁多态性。对于与疾病有流行病学关联的菌株,这些观察结果是成立的。发现inv和ail基因座都明确位于染色体上。包括其他侵袭性生物在内的其他属均没有与inv或ail同源的DNA。这些数据支持了ail基因座编码一种可能参与发病机制的小肠结肠炎耶尔森菌侵袭因子的假说。