IL-10 prevents liver necrosis during murine infection with Trichinella spiralis.

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.