Nod-like receptors (NLRs) and the inflammasome complex have significant
roles in regulating the innate immune system against bacterial and viral pathogens and
have attracted significant attention to their role in protozoan infections. Several
parasitic protozoan pathogens are the most prevalent that cause severe morbidity and
pose a significant health burden. In the present article, we discussed the most common
protozoan parasites and the roles of NLRs and inflammasomes against these parasites.
G. duodenalis, E. histolytica, T. vaginalis, Plasmodium parasite, T. cruzi, Schistosomes
parasite, T. gondii, and Leishmania spp. activate the NLRP3 inflammasome. The
NLRP3 inflammasome protects the host in Giardia, T. cruzi, and E. histolytica infections. Also, its protective role in the case of Trichomonas infection has been suggested,
but more studies are needed. However, NLRP3 induces pathology during Schistosomes
and Malaria parasite infection. In T. gondii infection, NLRP3 causes inflammation and
limits the parasite load burden and propagation. This provides a new dimension in the
research on the role and exact mechanism of NLRP3 during T. gondii infection. The
NLRP3 inflammasome protects the host by clearing the parasitic load; NLRP3 provides
resistance toward some Leishmania spp. It alleviates the host's parasitic burden of L.
amazonensis and L. major. However, L. major or L. donovani induces chronic nonhealing infection-promoting lesion development. These contrary reports warrant more
research on Leishmaniasis. For developing new treatment strategies, studying the role
of NLRP3 in the host defense and inflammatory pathology is crucial in parasitic
protozoan infection.
Keywords: IL-1β, IL-18, NLRP3, Protozoan infection.
