Fig. 1.

Immunopathogenesis of Bt-induced atopic asthma in the IL-33/NLRP3/CASP1 route. The contact of Bt with cells of the aerial epithelium results in damage and consequent release of IL-33. This, in turn, favors the Th2 response profile by activating several innate and adaptive immune cells, with high production of proinflammatory cytokines, also increasing degranulation and specific IgE production. On the other hand, activation of the intracellular NLRP3 receptor, present in the cytoplasm of the cells involved in this response, results in NLRP3 inflammasome formation and Casp-1 release. Casp-1 acts by inhibiting the IL-33 action and, consequently, attenuates the inflammation caused by this cytokine in airway.