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The intestinal protozoan parasite  Entamoeba histolytica  ( Eh ) causes amebiasis associated with severe diarrhea and/or liver abscess.  Eh  pathogenesis is multifactorial requiring both parasite virulent molecules and host-induced innate immune responses.  Eh -induced host pro-inflammatory responses plays a critical role in disease pathogenesis by causing damage to tissues allowing parasites access to systemic sites.  Eh  cyclooxygenase ( Eh Cox) derived prostaglandin E 2  stimulates the chemokine IL-8 from mucosal epithelial cells that recruits neutrophils to the site of infection to exacerbate disease. At present, it is not known how  Eh Cox is regulated or whether it affects the expression of other proteins in  Eh . In this study, we found that gene silencing of  Eh Cox ( EhCoxgs ) markedly increased endogenous cysteine protease (CP) protein expression and virulence without altering CP gene transcripts. Live virulent  Eh  pretreated with arachidonic acid substrate to enhance PGE 2  production or aspirin to inhibit  Eh Cox enzyme activity or addition of exogenous PGE 2  to  Eh  had no effect on  Eh CP activity. Increased CP enzyme activity in  EhCoxgs  was stable and significantly enhanced erythrophagocytosis, cytopathic effects on colonic epithelial cells and elicited pro-inflammatory cytokines in mice colonic loops. Acute infection with  EhCoxgs  in colonic loops increased inflammation associated with high levels of myeloperoxidase activity. This study has identified  Eh Cox protein as one of the important endogenous regulators of cysteine protease activity. Alterations of CP activity in response to Cox gene silencing may be a negative feedback mechanism in  Eh  to limit proteolytic activity during colonization that can inadvertently trigger inflammation in the gut.

Entamoeba histolytica Cyclooxygenase-Like Protein Regulates Cysteine Protease Expression and Virulence