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Role of inflammasomes in innate host defense against Entamoeba histolytica
Author(s) -
Begum Sharmin,
Gorman Hayley,
Chadha Attinder,
Chadee Kris
Publication year - 2020
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.3mr0420-465r
Subject(s) - entamoeba histolytica , inflammasome , biology , innate immune system , immune system , mucus , cathelicidin , immunology , microbiology and biotechnology , virulence , pathogenesis , caspase , inflammation , apoptosis , genetics , programmed cell death , gene , ecology
Intestinal amebiasis is the disease caused by the extracellular protozoan parasite Entamoeba histolytica ( Eh ) that induces a dynamic and heterogeneous interaction profile with the host immune system during disease pathogenesis. In 90% of asymptomatic infection, Eh resides with indigenous microbiota in the outer mucus layer of the colon without prompting an immune response. However, for reasons that remain unclear, in a minority of the Eh ‐infected individuals, this fine tolerated relationship is switched to a pathogenic phenotype and advanced to an increasingly complex host‐parasite interaction. Eh disease susceptibility depends on parasite virulence factors and their interactions with indigenous bacteria, disruption of the mucus bilayers, and adherence to the epithelium provoking host immune cells to evoke a robust pro‐inflammatory response mediated by inflammatory caspases and inflammasome activation. To understand Eh pathogenicity and innate host immune responses, this review highlights recent advances in our understanding of how Eh induces outside‐in signaling via Mϕs to activate inflammatory caspases and inflammasome to regulate pro‐inflammatory responses.