Ruiz-Bravo A, Moreno E, Jiménez-Valera M
Departamento de Microbiologia, Facultad de Farmacia, Universidad de Granada, 18071 Granada, Spain.
Microbiology (Reading). 2001 Nov;147(Pt 11):3165-9. doi: 10.1099/00221287-147-11-3165.
Yersinia enterocolitica serotype O9 may cause a persistent intestinal infection with few or no symptoms in humans and in BALB/c mice. The present study demonstrated profound alterations in the immune status of BALB/c mice infected with Y. enterocolitica O9. Infected mice developed splenomegaly and phenotypic analysis of spleen cells revealed increases in CD3+ total T cells, CD4+ helper T cells, CD8+ cytotoxic T cells and CD11b+ phagocytic cells. Spleen cells from infected mice exhibited impaired responses to mitogens and suppressed the proliferation of normal splenocytes in response to mitogens. Suppression of responses to concanavalin A and heat-killed yersiniae was associated with increased production of gamma interferon and reactive nitrogen intermediates. Y. enterocolitica-infected mice resisted challenge with a lethal dose of the intracellular pathogen Listeria monocytogenes. These findings suggest that infection of mice with Y. enterocolitica O9 induces gamma-interferon-secreting cells that promote macrophage activation, mediating resistance to infection with L. monocytogenes, and macrophage production of reactive nitrogen intermediates, which results in in vitro inhibition of lymphocyte response to mitogens.
小肠结肠炎耶尔森菌O9血清型可在人类和BALB/c小鼠中引起持续的肠道感染，症状很少或没有症状。本研究表明，感染小肠结肠炎耶尔森菌O9的BALB/c小鼠免疫状态发生了深刻变化。受感染小鼠出现脾肿大，对脾细胞的表型分析显示，CD3⁺总T细胞、CD4⁺辅助性T细胞、CD8⁺细胞毒性T细胞和CD11b⁺吞噬细胞增加。来自受感染小鼠的脾细胞对丝裂原的反应受损，并抑制正常脾细胞对丝裂原的增殖反应。对刀豆球蛋白A和热灭活耶尔森菌反应的抑制与γ干扰素和活性氮中间体产量增加有关。感染小肠结肠炎耶尔森菌的小鼠对致死剂量的细胞内病原体单核细胞增生李斯特菌具有抵抗力。这些发现表明，用小肠结肠炎耶尔森菌O9感染小鼠可诱导分泌γ干扰素的细胞，促进巨噬细胞活化，介导对单核细胞增生李斯特菌感染的抵抗力，以及巨噬细胞产生活性氮中间体，这导致体外淋巴细胞对丝裂原反应受到抑制。
