Infection Strategies of Intestinal Parasite Pathogens and Host Cell Responses

Abstract

Giardia lamblia, Cryptosporidium sp., and Entamoeba histolytica are important pathogenic intestinal parasites and are amongst the leading causes worldwide of diarrheal illness in humans. Diseases caused by these organisms, giardiasis, cryptosporidiosis, and amoebiasis, respectively, are characterized by self-limited diarrhea but can evolve to long-term complications. The cellular and molecular mechanisms underlying the pathogenesis of diarrhea associated with these three pathogens are being unraveled, with knowledge of both the strategies explored by the parasites to establish infection and the methods evolved by hosts to avoid it. Special attention is being given to molecules participating in parasite–host interaction and in the mechanisms implicated in the diseases’ pathophysiologic processes. This review focuses on cell mechanisms that are modulated during infection, including gene transcription, cytoskeleton rearrangements, signal transduction pathways, and cell death.

Cryptosporidium parvumdisrupts intestinal epithelial barrier function via altering expression of key tight junction and adherens junction proteins

“…Several diarrhoeal pathogens have been shown to disrupt AJCs in in vitro and in vivo models of infection (Groschwitz & Hogan, 2009;Nusrat et al, 2001;Vogelmann et al, 2004). Although limited studies demonstrated disrupted barrier function in cryptosporidiosis (Di Genova & Tonelli, 2016;Roche et al, 2000), very little is known about the alterations in the expression and/or assembly of TJ and AJ proteins and the underlying mechanisms. Because CP is known to infect and invade the cells of small intestinal epithelium, we used post-confluent Caco2 cell monolayers, morphologically and functionally mimicking the small intestinal mucosal barrier (Hidalgo, Raub, & Borchardt, 1989;Pignata, Maggini, Zarrilli, Rea, & Acquaviva, 1994), to examine the effects of infection by the parasite.…”

“…Few earlier studies showed decreased transepithelial resistance (TER) and increased paracellular permeability following Cryptosporidium parvum (CP) infection of intestinal epithelial cells in vitro or in vivo (Di Genova & Tonelli, 2016;Roche, Martins, Cosme, Fayer, & Guerrant, 2000). However, very little is known about the mechanisms of impaired barrier function or the effects on the expression of TJ and AJ assembly proteins in response to Cryptosporidium infection.…”

Multilocus typing of Cryptosporidium spp. in young calves with diarrhea in Korea

“…When the data were analyzed according to the type of diarrhea, there was low prevalence of C. parvum in calves with hemorrhagic diarrhea. Although the pathogenesis of Cryptosporidium remains unclear, Cryptosporidium is not considered to cause hemorrhagic diarrhea (Cho and Yoon, 2014;Di Genova and Tonelli, 2016) and appears to have a low association with this condition.…”

Effects of Enteromyxum spp. (Myxozoa) infection in the regulation of intestinal E‐cadherin: Turbot against gilthead sea bream

“…The immunohistochemical results indicate a change in the distribution pattern of E‐cadherin in turbot, with loss of homogeneity and enhanced presence at the enterocyte–parasite interface. In other parasitosis leading to intestinal barrier dysfunction, the pathogenesis involves the disassembly of cell–cell junctions and cytoskeleton, including the relocation of junctional proteins (Di Genova & Tonelli, ). As well, oxidative stress was demonstrated to induce redistribution of E‐cadherin and other junctional proteins, causing an increment in intestinal permeability in mice (Rao, Basuroy, Rao, Karnaky, & Gupta, ).…”