Autenrieth I B, Beer M, Hantschmann P, Preger S, Vogel U, Heymer B, Heesemann J
Institute for Hygiene and Microbiology, University of Würzburg, Germany.
Zentralbl Bakteriol. 1993 Apr;278(2-3):383-95. doi: 10.1016/s0934-8840(11)80855-8.
Resistance of mice against infection with Yersinia enterocolitica has been shown to be related neither to the Ity locus coding for resistance against infection with Salmonella typhimurium and other pathogens nor to the H-2 locus. From other mouse infection models, e.g., murine leishmaniasis, there is evidence that a different T cell-dependent regulation of the host immune response in various inbred strains of mice determines the susceptibility to the infectious agent. However, until recently, little was known about the cellular immune response against Y. enterocolitica. Thus, in a first approach we used the highly virulent Y. enterocolitica strain WA of serotype O:8 and different inbred strains of mice (C57 BL/6, Balb/c and athymic T cell-deficient C57 BL/6 nude mice) to investigate the cell-mediated immunity against parenteral infection. Comparison of the median lethal dose and of the net-bacterial growth in the spleens of infected mice indicated that Balb/c mice could be considered as Yersinia-susceptible whereas C57 BL/6 mice were relatively resistant. However, in contrast to normal C57 BL/6, athymic T cell-deficient C57 BL/6 nude mice have proved to be highly susceptible to Yersinia infection suggesting that T cells are required for the elimination of the pathogen. This conclusion was supported by histomorphological and immunohistological results indicating that T lymphocytes were present in Yersinia-induced tissue lesions. Moreover, the adoptive transfer of Yersinia-specific T cell lines and clones into naive animals mediated significant protection against the pathogen in both Yersinia-resistant C57 BL/6 and in Yersinia-susceptible Balb/c mice. These findings emphasize an important role of T lymphocytes in the host response against Y. enterocolitica infection.
已证明小鼠对小肠结肠炎耶尔森菌感染的抵抗力既与编码对鼠伤寒沙门氏菌和其他病原体感染抵抗力的Ity基因座无关，也与H-2基因座无关。从其他小鼠感染模型，如鼠利什曼病模型中，有证据表明，在各种近交系小鼠中，宿主免疫反应存在不同的T细胞依赖性调节，这决定了对感染因子的易感性。然而，直到最近，人们对针对小肠结肠炎耶尔森菌的细胞免疫反应仍知之甚少。因此，在第一步研究中，我们使用了血清型为O:8的高毒力小肠结肠炎耶尔森菌菌株WA和不同的近交系小鼠（C57 BL/6、Balb/c和无胸腺T细胞缺陷的C57 BL/6裸鼠）来研究针对肠道外感染的细胞介导免疫。对感染小鼠脾脏中半数致死剂量和细菌净生长的比较表明，Balb/c小鼠可被视为对耶尔森菌易感，而C57 BL/6小鼠相对有抵抗力。然而，与正常的C57 BL/6小鼠不同，无胸腺T细胞缺陷的C57 BL/6裸鼠已被证明对耶尔森菌感染高度易感，这表明T细胞是清除病原体所必需的。组织形态学和免疫组织学结果支持了这一结论，这些结果表明T淋巴细胞存在于耶尔森菌诱导的组织损伤中。此外，将耶尔森菌特异性T细胞系和克隆过继转移到未感染的动物中，在对耶尔森菌有抵抗力的C57 BL/6小鼠和对耶尔森菌易感的Balb/c小鼠中均介导了对病原体的显著保护作用。这些发现强调了T淋巴细胞在宿主对小肠结肠炎耶尔森菌感染反应中的重要作用。
