Athanazio Daniel A, Santos Cleiton S, Santos Andréia C, McBride Flávia W C, Reis Mitermayer G
Gonçalo Moniz Research Centre, Oswaldo Cruz Foundation, Ministry of Health, Salvador, Brazil.
Acta Trop. 2008 Jan;105(1):95-8. doi: 10.1016/j.actatropica.2007.09.004. Epub 2007 Sep 29.
Only recently, knockout mouse models were applied in studies on the pathogenesis of leptospirosis. Current data suggest an important role of innate immunity receptors and interferon gamma dependant cellular response on protection. It is not clear, however, whether T helper cell polarization influences on outcome of leptospiral infection. We report findings of experimental infection of C57BL/6 (interferon gamma or tumor necrosis factor alpha receptor deficient) and BALB/c (interleukin 4 deficient) mice infected by pathogenic Leptospira interrogans serovar Copenhageni. Specific cytokine gene deficiency had no impact on outcome since all animals survived. TNFR knockout mice, however, exhibited more severe residual renal inflammation during convalescence thus suggesting this cytokine is important in early control of infection, protecting kidneys from relevant pathology.
直到最近,基因敲除小鼠模型才被应用于钩端螺旋体病发病机制的研究。目前的数据表明,先天免疫受体和干扰素γ依赖性细胞反应在保护方面发挥着重要作用。然而,尚不清楚辅助性T细胞极化是否会影响钩端螺旋体感染的结果。我们报告了对感染致病性问号钩端螺旋体哥本哈根血清型的C57BL/6(干扰素γ或肿瘤坏死因子α受体缺陷型)和BALB/c(白细胞介素4缺陷型)小鼠进行实验性感染的研究结果。特定细胞因子基因缺陷对结果没有影响,因为所有动物都存活了下来。然而,肿瘤坏死因子受体基因敲除小鼠在恢复期表现出更严重的残余肾炎症,因此表明这种细胞因子在感染的早期控制中很重要,可以保护肾脏免受相关病理损害。