Abstract
Malaria predisposes to concomitant bacteremia, resulting in increased mortality risk. Previous studies indicated that malaria causes structural changes in the intestine, induces tolerogenic immune responses, inhibits neutrophil recruitment, suppresses innate synthesis of IFN-γ, dysregulates mast cells (MCs) and basophils, and induces Th2-type immune responses. These can reduce parasite control while increasing enteropathogenic dissemination. Moreover, there is growing evidence that Th2 immunity, while protecting the host from overwhelming inflammation, may also contribute to increased parasite transmission. This review explores the roles of the regulatory immune response in bacterial coinfections and parasite transmission in malaria.