Amebiasis is an
infectious disease caused by Entamoeba histolytica, an anaerobic protozoan parasite, and is a major public health problem worldwide, particularly in areas with inadequate sanitation and poor hygiene. Th1 responses, represented by
interferon gamma (IFN-γ), play a protective role by clearing the amebae from the gut, whereas Th2 responses are responsible for
chronic infection. Th17 responses preconditioned by vaccination or by modulating the intestinal microbiome protect mice from the settlement of E. histolytica. However, the role of
interleukin-17A (IL-17A), which is upregulated during the natural course of
intestinal amebiasis, has not been clarified. The aim of this study was to investigate the role of
IL-17A during
intestinal amebiasis in a mouse model.
IL-17A knockout and wild-type CBA/J mice were challenged intracecally with 2×106E. histolytica trophozoites, and their
infection, pathology, and immune responses were monitored. Neither the initial settlement of E. histolytica nor the
inflammation of the cecum was affected by the absence of
IL-17A for week 1, but the
infection rate and parasite burden declined in a late stage of
infection, accompanied by an increased IFN-γ/IL-4 ratio. Therefore,
IL-17A contributes to the persistence of E. histolytica and modulates the immune response, including the IFN-γ/IL-4 ratio, which may be responsible for the reduction of the parasite burden in the
IL-17A knockout mice during the chronic phase of
intestinal amebiasis.