Interleukin 33 mediates type 2 immunity and inflammation in the central nervous system of mice infected with Angiostrongylus cantonensis.

Abstract

Angiostrongylus cantonensis can induce central nervous system (CNS) injury and cause human eosinophilic meningitis. The CNS has been found to have high expression of interleukin 33 (IL-33), which promotes the pathogenesis of T-helper 2 (Th2)-related disease. Given the predominantly type 2 response induced by A. cantonensis-infected mice and human, it is likely that IL-33 may play a role in aiding this process. We report here that IL-33 protein and ST2L messenger RNA (mRNA) transcripts in the brains were upregulated during A. cantonensis infection and that both splenocytes and brain mononuclear cells became IL-33 responsive and produced interleukin 5 and interleukin 13. Furthermore, administration of IL-33 to A. cantonensis-infected mice enhanced ST2L expression and cytokine production. Interestingly, brain IL-33 protein and ST2L mRNA levels were elevated 14-21 days after infection in BALB/c mice, compared with C57BL/6 mice. Thus, our data indicate that IL-33 produced in the brain may function as an inflammatory mediator in eosinophilic meningitis induced by A. cantonensis.