부산대학교 도서관

The protozoan parasite Entamoeba histolytica is the causative agent of amebiasis, an infection that manifests as colitis and, in some cases, liver abscess. A better understanding of host protective factors is key to developing an effective remedy. Recently, significant advances have been made in understanding the mechanisms of MUC2 production by goblet cells upon amebic infection, regulation of antimicrobial peptide production by Paneth cells, the interaction of commensal microbiota with immune stimulation, and host genetics in conferring protection from amebiasis. In addition to host pathways that may serve as potential therapeutic targets, significant progress has also been made with respect to development of a vaccine against amebiasis. Here, we aim to highlight the current understanding and knowledge gaps critically. Vesicle-mediated exocytosis of MUC2 is critical in providing protection against tissue damage, and MUC2 regulates antimicrobial peptide production by Paneth cells during Entamoeba histolytica infection. While certain pathobionts can defend the ameba from oxidative stress in the colon, other commensal microbiota can protect the host by controlling the recruitment of neutrophils. Amebic infection downregulates interleukin (IL)-25 production in mice and humans. Exogenous treatment with IL-25 induces eosinophilia to confer protection. Children with a polymorphism in transcription factor cAMP response element modulator (CREM), and CREM knockout mice, are more susceptible to amebiasis. Vaccination with amebic surface protein LecA combined with Toll-like receptor (TLR)4 and TLR7/8 agonists induces a robust mucosal IgA, interferon (IFN)-γ, and IL-17a response to provide protection from amebiasis. [ABSTRACT FROM AUTHOR]