Animal Models of Helminth Exposure

Exposing mice to H. polygyrus also changes the host s intestinal innate immune system. Once exposed to worms, the intestinal immune system is less able to support an adaptive immune 

IL17 and IL12p40 at least partly drive colitis in ILIO mice as demonstrated by antibody neutralization experiments. IL12p40 is the shared component of IL12 and IL23, which drive IFNy and IL17, respectively. Worm infoction blocks expression of all three in the gut. This could underlay the strong protection from cohtis seen in worm colonization. 

Exposure to helminths inhibits central nervous system inflammation in experimental autoimmune encephahtis (EAE). a rodent model of MS. Exposure of mice to viable S. mansoni or dead (freeze-thawed) S. mansoni s protects from EAE. Schistosome exposure reduces proinflammatory IL12/23p40, IFNy and TNFa and promotes r ulatory TGPp, ILIO and IL4 expression by splenocytes and CNS immune cells. Protection against EAE appears to require intact IL4 signaling.  

Colonization with helminths prevent onset of diabetes in the NOD murine model of TID. NOD mice exposed to S. mansoni are protected from developing diabetes. Schistosome egg or antigen e q osure induces immune regulatory ILIO and augments NKT cell activity that may help prevent insulinitis. Colonization with T. spiralis or H. polygyrus also inhibits diabetes in NODmice.  

Reactive airway disease improves with helminth exposure in murine models of asthma. Colonization of mice with male S. mansoni protects against airway hyperreactivity but this protective effect is lost with productive (male and female worm) infection. Mice colonized only with male worms developed a modified immune response in the lung with decreased allergen-specific IL5 and increased ILIO producticxi compared to uninfected mice. This decrease in allergen-specific IL5 release is similar to that reported in people with productive S. mansoni infections.  

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