Role of NLRP3 in Protozoan Parasitic Infections

Abstract

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.