Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice

Toxocariasis
is a neglected disease caused by Toxocara canis, which has 19% worldwide
seroprevalence, and is associated with socioeconomic, geographic and
environmental factors. Humans become infected by accidental ingestion of T. canis eggs present in contaminated
food, water or soil. After ingestion, the larvae hatch in the intestine and can
reach various tissues such as liver, lung and brain. Helminth infections
usually trigger a Th2 immune response in the host, by releasing cytokines such
as IL-4, IL-5, IL-13 and IL-33. IL-33 is an alarmin that binds to the ST2
receptor, and some studies have observed an increase in this cytokine in
toxocariasis, however there are no studies regarding the IL-33/ST2 role in this
infection. Thus, we evaluated the influence of this pathway by analyzing
immunological and pathophysiological aspects in T. canis-infected mice. Our results
demonstrated that the IL-33/ST2 pathway is related to parasite burden on the
liver and brain and also increases the number of eosinophils in the blood and
tissues. In addition, it involved with the pulmonary immune response and granulomas
with impact in lung function. In
conclusion, the IL-33/ST2 pathway governs the host susceptibility to T.
canis in mice.