Bliss Susan K, Alcaraz Ana, Appleton Judith A
James A. Baker Institute for Animal Health, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
J Immunol. 2003 Sep 15;171(6):3142-7. doi: 10.4049/jimmunol.171.6.3142.
Infection with Trichinella spiralis rarely leads to significant morbidity. In this study, we show that IL-10 knockout mice infected with this parasite develop extensive areas of coagulative necrosis in the liver, and newborn larvae are required for lesion formation. Histopathological examination revealed that the hepatic inflammatory infiltrate was mixed but dominated by eosinophils. Accordingly, infected IL-10 knockout mice displayed a marked eosinophilia. IL-10 was expressed during infection in mesenteric lymph node populations and liver tissue. Analysis of cytokine profiles revealed a codominant expression of type 1 and 2 mediators that was enhanced in the absence of IL-10. Additionally, CD11c(+) MHC class II(+) cells were increased in mesenteric lymph nodes of IL-10 knockout mice, suggesting a possible link between IL-10 and dendritic cell trafficking. Nevertheless, there were no significant differences in mortality or parasite burdens between the strains of mice, indicating that IL-10 is necessary to control the host's inflammatory response but does not impact establishment of the parasite. Expression of IL-10 appears to be an adaptation used by the liver to protect itself from damage caused by migrating newborn larvae.
旋毛虫感染很少导致严重发病。在本研究中，我们发现感染该寄生虫的白细胞介素-10（IL-10）基因敲除小鼠肝脏出现大面积凝固性坏死，且病变形成需要新生幼虫。组织病理学检查显示，肝脏炎性浸润为混合性，但以嗜酸性粒细胞为主。相应地，感染的IL-10基因敲除小鼠表现出明显的嗜酸性粒细胞增多。IL-10在肠系膜淋巴结群体和肝脏组织感染期间表达。细胞因子谱分析显示，在缺乏IL-10的情况下，1型和2型介质共显性表达增强。此外，IL-10基因敲除小鼠肠系膜淋巴结中CD11c(+)MHC II类(+)细胞增加，提示IL-10与树突状细胞迁移之间可能存在联系。然而，不同品系小鼠在死亡率或寄生虫负荷方面没有显著差异，这表明IL-10对于控制宿主的炎症反应是必要的，但不影响寄生虫的建立。IL-10的表达似乎是肝脏用于保护自身免受新生幼虫迁移所致损伤的一种适应性机制。
