Bolton Alex J, Osborne Michael P, Wallis Tim S, Stephen John
Molecular Microbiology and Cell Biology Group, School of Biological Sciences1 and Department of Physiology, The Medical School2, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Institute for Animal Health, Compton, Newbury RG20 7NN, UK3.
Microbiology (Reading). 1999 Sep;145 ( Pt 9):2431-2441. doi: 10.1099/00221287-145-9-2431.
Quantitative experiments on the interaction of Salmonella choleraesuis and Salmonella dublin with porcine and bovine intestinal epithelia yielded no evidence to suggest that host restriction of S. choleraesuis and S. dublin for pigs and calves respectively could be explained in terms of the patterns of intestinal invasion observed in ligated ileal loops in vivo, at 3 h after challenge. No evidence was found to support the idea that Peyer's patches, or specifically M cells, are the major route of entry for these serotypes in vivo. Three hours after loop inoculation, each serotype was recovered in comparable numbers from either absorptive or Peyer's patch mucosae present in the same ileal loop, indicating that both types of tissue are involved in the early stages of the enteropathogenic process induced by both serotypes. More detailed transmission electron microscopic (TEM) analyses of follicle-associated epithelia (FAE) challenged with S. choleraesuis showed that in the same region of FAE, organisms invaded both M cells and enterocytes directly; comparable detailed TEM studies with S. dublin could not be carried out because of the tissue-destructive properties of this serotype. S. dublin was clearly more histotoxic than S. choleraesuis as had previously been found in rabbits: this difference is almost certainly due to a tissue-damaging toxin which is neither host nor gut-tissue specific. The tissue-destructive potential of S. dublin has profound implications for the measurement of and the assignment of significance to the invasiveness of S. dublin. S. dublin was nearly always seen entering gut cells in micro-colonies whereas S. choleraesuis entered mainly as single organisms or small groups of two or three.
关于猪霍乱沙门氏菌和都柏林沙门氏菌与猪和牛肠道上皮细胞相互作用的定量实验结果表明,没有证据显示猪霍乱沙门氏菌和都柏林沙门氏菌分别对猪和牛的宿主限制能够用在体内回肠结扎环中于攻毒后3小时观察到的肠道侵袭模式来解释。没有发现证据支持派尔集合淋巴结或特定的M细胞是这些血清型在体内主要进入途径的观点。环接种3小时后,在同一个回肠环中的吸收性黏膜或派尔集合淋巴结黏膜中回收得到的每种血清型菌数量相当,这表明两种类型的组织都参与了这两种血清型诱导的肠道致病过程的早期阶段。对受猪霍乱沙门氏菌攻击的滤泡相关上皮(FAE)进行更详细的透射电子显微镜(TEM)分析显示,在FAE的同一区域,细菌既侵袭M细胞也直接侵袭肠上皮细胞;由于该血清型具有组织破坏性,无法对都柏林沙门氏菌进行类似的详细TEM研究。正如之前在兔子身上发现的那样,都柏林沙门氏菌明显比猪霍乱沙门氏菌更具组织毒性:这种差异几乎肯定是由于一种既非宿主特异性也非肠道组织特异性的组织损伤毒素所致。都柏林沙门氏菌的组织破坏潜力对都柏林沙门氏菌侵袭性的测量及重要性的判定具有深远影响。都柏林沙门氏菌几乎总是以微菌落形式进入肠道细胞,而猪霍乱沙门氏菌主要以单个菌或两三个菌的小群体形式进入。