Interleukin‐5 deficient mice exhibit impaired host defence against challenge Trichinella spiralis infections

Enteric nematode infections are characterized by both peripheral and tissue eosinophilia. The cytokine interleukin (IL)-5 is considered a critical factor in the proliferation and recruitment of eosinophils, however, studies suggest it plays little role in host defence, at least during primary Trichinella spiralis infections. Less is known concerning its role in host defence or in the inflammatory response that develops against challenge infections with the same parasite. We examined these questions by infecting IL-5 deficient and wild-type mice, with T. spiralis parasites. Both strains expelled the primary infection by day 21. Forty days after the primary infection, we challenged the mice with a second T. spiralis infection and counted tissue eosinophils and worms in the intestine. While wild-type mice developed a large tissue eosinophilia, IL-5 deficient mice showed little increase in eosinophil numbers within the intestine. Throughout the challenge infection, significantly larger worm burdens were recovered from IL-5 deficient mice, and worm expulsion was also significantly slower (day 21) compared to wild-type mice (day 14). Thus, unlike in a primary infection, IL-5 is not only essential for the onset of intestinal eosinophilia, but also makes a significant contribution to enteric host defence during challenge T. spiralis infections.