Mechanisms of the airway hyperresponsiveness induced by Strongyloides venezuelensis infection in rats: role of capsaicin-sensitive neurons.

Strongyloides venezuelensis migrates through the lungs and induces airway hyperresponsiveness (AHR). The present study evaluated the role of C-fibers in mediating airway inflammation and AHR after infection of rats with S. venezuelensis.

Prevention of changes in airway function facilitates Strongyloides venezuelensis infection in rats.

Alterations in lung function and pulmonary symptoms have been described in patients infected with helminths with a lung cycle. We have previously shown that infection with the nematode Strongyloides venezuelensis induced a significant increase in airway hyperreactivity in infected rats. The aim of the present study was to test the hypothesis that bronchodilation during the lung phase of parasite migration would favor completion of the life cycle and infection indices.

Expression of IL-4 receptor on non-bone marrow-derived cells is necessary for the timely elimination of Strongyloides venezuelensis in mice, but not for intestinal IL-4 production.

In rodents and in humans, Strongyloides infection induces an immune response which is predominantly Th2 in nature. In an attempt to understand the role of the IL-4R/STAT6 signaling pathway, the pathway activated by the Th2 cytokines IL-4 and IL-13, in the induction of protection during Strongyloides venezuelensis infection, we have carried out experiments in mice lacking the IL-4Ralpha chain. Experiments were also carried out in STAT6 (STAT6(-/-)) and IL-12-deficient (IL-12(-/-)) mice for comparison.