Parasitology Unit, Department of Pathology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand.
Exp Parasitol. 2010 Nov;126(3):415-20. doi: 10.1016/j.exppara.2010.01.019. Epub 2010 Feb 1.
The function of mitogen-activated protein kinase (MAPK) family member c-Jun N-terminal kinase (JNK)-2 in resistance and pathology during infection has not been greatly studied. Here, we employed Jnk2(-/-) mice to investigate the role of JNK2 in resistance and immunity during oral infection with the protozoan pathogen Toxoplasma gondii. We found increased host resistance in the absence of JNK2 as determined by lower parasite burden and increased host survival. Lack of JNK2 also correlated with decreased neutrophil recruitment to the intestinal mucosa and less pathology in the small intestine. In the absence of JNK2, IL-12 production was slightly but significantly increased in restimulated splenocyte populations as well as in purified splenic dendritic cell cultures. These results provide evidence that expression of JNK2 plays a role in T. gondii-induced immunopathology, at the same time in promoting susceptibility to this parasitic pathogen.
丝裂原活化蛋白激酶（MAPK）家族成员 c-Jun N 末端激酶（JNK）-2 在感染过程中的耐药性和病理学功能尚未得到深入研究。在这里，我们利用 Jnk2(-/-) 小鼠来研究 JNK2 在感染原生动物病原体弓形虫时对抵抗和免疫的作用。我们发现，在没有 JNK2 的情况下，宿主的抵抗力增强，寄生虫负荷降低，宿主存活率提高。缺乏 JNK2 也与肠道黏膜中性粒细胞募集减少和小肠病变减少有关。在缺乏 JNK2 的情况下，再刺激脾细胞群体以及纯化的脾树突状细胞培养物中，IL-12 的产生略有但显著增加。这些结果表明 JNK2 的表达在弓形虫诱导的免疫病理学中发挥作用，同时也促进了对这种寄生虫病原体的易感性。
