Impaired clearance of primary but not secondary Brugia infections in IL-5 deficient mice

Abstract Eosinophilia in blood and tissues has been strongly associated with helminth infections for over a century. In vivo depletion of IL-5, a cytokine crucially involved in eosinophilopoiesis with an antibody or through genetic manipulation, reproducibly abrogates helminth-induced eosinophilia, but renders mice permissive only in some models of parasite infection. In the current study, we compared the ability of IL-5 −/− and B6 +/+ mice to clear intraperitoneal infections with Brugia pahangi L3. IL-5 −/− mice had statistically significantly higher worm burdens than B6 +/+ . This was true for primary infections, in young as well as old mice, suggesting that IL-5 deficient mice are more permissive to Brugian infections. This increase in permissiveness seemed to correlate well with the drastically reduced eosinophil numbers in the peritoneal cavity, the site of infection. In secondary infections, primed IL-5 −/− mice cleared infections in an accelerated manner, comparable with B6 +/+ mice. These observations suggest that IL-5 induced eosinophilia is more important in the control of a primary infection in naive mice than a secondary infection in primed mice. Index Descriptors and Abbreviations: Brugia pahangi ; Inbred mice; Parasite infection; Peritoneal inflammation; C57BL/6J; IL5; IL-5 −/− ; Flowcytometry; Eosinophils; B1 B cells