Intestinal Invasion by Entamoeba histolytica

Solaymani-Mohammadi, Shahram; Petri, William A.

doi:10.1007/978-0-387-78267-6_18

Cited by 11 publications

(5 citation statements)

References 76 publications

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“…Several other factors contribute to the pathogenicity of Entamoeba histolytica and some may still await identification. Three important pathogenic factors that have been investigated and characterized are at molecular level: (1) the Gal/GalNAc adhesion, mediating adherence to host cells and contributing to amoebic resistance to complement, (2) the amoebapores, small peptides that produce pores in target membrane, and (3) cysteine proteinases that play a key role in Entamoeba histolytica tissue invasion, evasion of host defence, and parasite induction of inflammation [ 30 ]. Beyond doubt Entamoeba histolytica genome sequence and new molecular techniques will rapidly advance the understanding of the epidemiology and pathogenicity of amoebiasis.…”

Section: Amoebic Liver Abscess and Alcoholmentioning

confidence: 99%

Amoebic Liver Abscess and Indigenous Alcoholic Beverages in the Tropics

Kumanan

Sujanitha

Balakumar

et al. 2018

Journal of Tropical Medicine

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Amoebic liver abscess (ALA) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders. Whether the role of alcohol in the development of ALA is incidental and casual or whether alcohol is causally implicated has been debated. It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA. However, there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA. These factors include the role of alcohol in host immunity, parasitic proliferation, and invasion and in creating a conducive hepatic microenvironment. The contributory role of alcohol-induced increase in hepatic iron stores and lipid content is discussed. Late-stage liver disease with fibrosis seems to be protective for the development of ALA. Further research is necessary to elucidate the many possible mechanisms that predispose to hepatic amoebiasis, so that appropriate individual and population-based preventive measures can be implemented.

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Section: Amoebic Liver Abscess and Alcoholmentioning

confidence: 99%

Amoebic Liver Abscess and Indigenous Alcoholic Beverages in the Tropics

Kumanan

Sujanitha

Balakumar

et al. 2018

Journal of Tropical Medicine

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“…The TJ gate function in MDCK and Caco-2 cells suffered differential impact after the trophozoites and EhCP112 attack (Figure 3 ), supporting the distinct susceptibility of epithelial cell lines to trophozoites molecules. In in vivo studies, we need to have in mind that the host immune response plays a double role, modulating the damage that the parasite and its molecules produce (Petri, 2008 ; Mortimer and Chadee, 2010 ) and generating defense cells and molecules that could contribute to the tissue injure. To gain further insight on the E. histolytica damage produced on animal models, we investigated the effect of rEhCP112a on C57/BL6 mice, a strain susceptible to the trophozoites colonization (Kissoon-Singh et al, 2013 ).…”

Section: Resultsmentioning

confidence: 99%

Entamoeba histolytica EhCP112 Dislocates and Degrades Claudin-1 and Claudin-2 at Tight Junctions of the Intestinal Epithelium

Cuellar

Hernández-Nava

Garcı́a-Rivera

et al. 2017

Front. Cell. Infect. Microbiol.

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During intestinal invasion, Entamoeba histolytica opens tight junctions (TJs) reflected by transepithelial electrical resistance (TEER) dropping. To explore the molecular mechanisms underlying this, we studied in vitro and in vivo the damage produced by the recombinant E. histolytica cysteine protease (rEhCP112) on TJ functions and proteins. rEhCP112 reduced TEER in Caco-2 cells in a dose- and time-dependent manner; and EhCP112-overexpressing trophozoites provoked major epithelial injury compared to control trophozoites. rEhCP112 penetrated through the intercellular space, and consequently the ion flux increased and the TJs fence function was disturbed. However, macromolecular flux was not altered. Functional in vitro assays revealed specific association of rEhCP112 with claudin-1 and claudin-2, that are both involved in regulating ion flux and fence function. Of note, rEhCP112 did not interact with occludin that is responsible for regulating macromolecular flux. Moreover, rEhCP112 degraded and delocalized claudin-1, thus affecting interepithelial adhesion. Concomitantly, expression of the leaky claudin-2 at TJ, first increased and then it was degraded. In vivo, rEhCP112 increased intestinal epithelial permeability in the mouse colon, likely due to apical erosion and claudin-1 and claudin-2 degradation. In conclusion, we provide evidence that EhCP112 causes epithelial dysfunction by specifically altering claudins at TJ. Thus, EhCP112 could be a potential target for therapeutic approaches against amoebiasis.

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“…The mucosal surface of the intestinal tract represents a main entry point for various microbial pathogens. These microbial pathogens encounter natural innate barriers in the gut, including the mucus layer, in order to prevent potential pathogens or their immunomodulatory components/antigens to reach the underlying epithelium, a process known as non-immune exclusion ( 94 , 95 ). Mucins of the human gastrointestinal tract are highly glycosylated proteins and consist of an apomucin protein backbone (100-500 kDa) joined to oligosaccharides ( 96 ).…”

Section: Intestinal Epithelium As First Defense Layer Against ...mentioning

confidence: 99%

Mucosal Defense Against Giardia at the Intestinal Epithelial Cell Interface

Solaymani-Mohammadi

2022

Front. Immunol.

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Human giardiasis, caused by the protozoan parasite Giardia duodenalis (syn. Giardia lamblia, Giardia intestinalis, Lamblia intestinalis), is one of the most commonly-identified parasitic diseases worldwide. Chronic G. duodenalis infections cause a malabsorption syndrome that may lead to failure to thrive and/or stunted growth, especially in children in developing countries. Understanding the parasite/epithelial cell crosstalk at the mucosal surfaces of the small intestine during human giardiasis may provide novel insights into the mechanisms underlying the parasite-induced immunopathology and epithelial tissue damage, leading to malnutrition. Efforts to identify new targets for intervening in the development of intestinal immunopathology and the progression to malnutrition are critical. Translating these findings into a clinical setting will require analysis of these pathways in cells and tissues from humans and clinical trials could be devised to determine whether interfering with unwanted mucosal immune responses developed during human giardiasis provide better therapeutic benefits and clinical outcomes for G. duodenalis infections in humans.

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Intestinal Invasion by Entamoeba histolytica

Cited by 11 publications

References 76 publications

Amoebic Liver Abscess and Indigenous Alcoholic Beverages in the Tropics

Amoebic Liver Abscess and Indigenous Alcoholic Beverages in the Tropics

Entamoeba histolytica EhCP112 Dislocates and Degrades Claudin-1 and Claudin-2 at Tight Junctions of the Intestinal Epithelium

Mucosal Defense Against Giardia at the Intestinal Epithelial Cell Interface

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