Interactions Between
            <i>Entarnoeba histolytica</i>
            , Bacteria and Intestinal Cells

Mirelman, David; Feingold, Carmela; Wexler, A; Bracha, Rivka

doi:10.1002/9780470720806.ch2

Cited by 21 publications

(17 citation statements)

References 38 publications

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“…Phagocytosis assays demonstrated a Ͼ80% reduction in the number of trophozoites containing bacteria when the bacterial prey lacked O-antigen, the outermost layer of LPS. This result is supported by previous research indicating that E. histolytica primarily engulfs Gram-negative pathogens (30). Other investigators have also demonstrated selective engulfment of bacteria by amoebae based upon bacterial O-antigen (31,32).…”

Section: Figsupporting

confidence: 80%

Evidence for a Bacterial Lipopolysaccharide-Recognizing G-Protein-Coupled Receptor in the Bacterial Engulfment by Entamoeba histolytica

et al. 2013

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Entamoeba histolytica is the causative agent of amoebic dysentery, a worldwide protozoal disease that results in approximately 100,000 deaths annually. The virulence of E. histolytica may be due to interactions with the host bacterial flora, whereby trophozoites engulf colonic bacteria as a nutrient source. The engulfment process depends on trophozoite recognition of bacterial epitopes that activate phagocytosis pathways. E. histolytica GPCR-1 (EhGPCR-1) was previously recognized as a putative G-protein-coupled receptor (GPCR) used by Entamoeba histolytica during phagocytosis. In the present study, we attempted to characterize EhGPCR-1 by using heterologous GPCR expression in Saccharomyces cerevisiae. We discovered that bacterial lipopolysaccharide (LPS) is an activator of EhGPCR-1 and that LPS stimulates EhGPCR-1 in a concentration-dependent manner. Additionally, we demonstrated that Entamoeba histolytica prefers to engulf bacteria with intact LPS and that this engulfment process is sensitive to suramin, which prevents the interactions of GPCRs and G-proteins. Thus, EhGPCR-1 is an LPS-recognizing GPCR that is a potential drug target for treatment of amoebiasis, especially considering the well-established drug targeting to GPCRs.

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Section: Figsupporting

confidence: 80%

Evidence for a Bacterial Lipopolysaccharide-Recognizing G-Protein-Coupled Receptor in the Bacterial Engulfment by Entamoeba histolytica

et al. 2013

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“…Working with E. histolytica , Mirelman and colleagues (1982, 1983) evidenced that interactions of amoebae of low pathogenicity with a variety of Gram-negative bacteria, mainly Escherichia coli strains, may be responsible for the increase in amoebic virulence. More recently, Galván-Moroyoqui et al (2008) demonstrated that phagocytosis of enteropathogenic bacteria strains (e.g., E. coli and Shigella dysenteriae ) in vitro co-cultured with E. histolytica and Entamoeba dispar augmented the cytopathic effect of E. histolytica and increased expression of Gal/GalNAc lectin on the amoebic surface and the cysteine proteinase activity.…”

Section: Protozoansmentioning

confidence: 99%

Interactions between parasites and microbial communities in the human gut

Berrilli¹,

Cave²,

Cavallero³

et al. 2012

Front. Cell. Inf. Microbio.

122

114

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The interactions between intestinal microbiota, immune system, and pathogens describe the human gut as a complex ecosystem, where all components play a relevant role in modulating each other and in the maintenance of homeostasis. The balance among the gut microbiota and the human body appear to be crucial for health maintenance. Intestinal parasites, both protozoans and helminths, interact with the microbial community modifying the balance between host and commensal microbiota. On the other hand, gut microbiota represents a relevant factor that may strongly interfere with the pathophysiology of the infections. In addition to the function that gut commensal microbiota may have in the processes that determine the survival and the outcome of many parasitic infections, including the production of nutritive macromolecules, also probiotics can play an important role in reducing the pathogenicity of many parasites. On these bases, there is a growing interest in explaining the rationale on the possible interactions between the microbiota, immune response, inflammatory processes, and intestinal parasites.

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“…Entamoeba histolytica, the causative organism of amoebic dysentery, has a TF-binding lectin that is essential for its pathogenicity, and it seems plausible that inflammatory bowel conditions that lead to increased mucosal TF expression could greatly increase susceptibility to invasive amoebiasis. It is also a reasonable hypothesis that sialidase-secreting bacteria in the colonic lumen could have a symbiotic relationship with E. histolytica and co-incubation of bacteria with E. histolytica can in some experimental circumstances be shown to increase pathogenicity [38], although bacteria can also reduce invasiveness of E. histolytica by releasing glycosidases and proteases that degrade the Entamoeba lectin that is essential for its adherence [39]. Alterations in the mucosa-associated microbiota have been reported both in inflammatory bowel disease and in colorectal cancer, particularly an increase in mucosa-associated Escherichia coli that have a characteristic adherent and invasive phenotype [40,41].…”

Section: Implications For Interaction With Pathogensmentioning

confidence: 98%

Lectin–epithelial interactions in the human colon

Rhodes

Campbell

2008

Biochemical Society Transactions

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Similar changes in glycosylation occur in the colonic epithelium in inflammatory conditions such as ulcerative colitis and Crohn's disease and also in colon cancer and precancerous adenomatous polyps. They include reduced length of O-glycans, reduced sulfation, increased sialylation and increased expression of oncofetal carbohydrate antigens, such as sialyl-Tn (sialylalpha2-6GalNAc), and the TF antigen (Thomsen-Friedenreich antigen) Galbeta1-3GalNAcalpha-Ser/Thr. The changes affect cell surface as well as secreted glycoproteins and mediate altered interactions between the epithelium and lectins of dietary, microbial or human origin. Different TF-binding lectins cause diverse effects on epithelial cells, reflecting subtle differences in binding specificities e.g. for sialylated TF; some of these interactions, such as with the TF-binding peanut lectin that resists digestion, may be biologically significant. Increased TF expression by cancer cells also allows interaction with the human galactose-binding lectin, galectin-3. This lectin has increased concentration in the sera of patients with metastatic cancer and binds TF on cancer cell surface MUC1 (mucin 1), causing clustering of MUC1 and revealing underlying adhesion molecules which promote adhesion to endothelium. This is likely to be an important mechanism in cancer metastasis and represents a valid therapeutic target. Tools are now available to allow fast and accurate elucidation of glycosylation changes in epithelial disease, characterization of their potential lectin ligands, whether dietary, microbial or human, and determination of the functional significance of their interactions. This should prove a very fruitful area for future research with relevance to infectious, inflammatory and cancerous diseases of the epithelia.

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Interactions Between Entarnoeba histolytica , Bacteria and Intestinal Cells

Cited by 21 publications

References 38 publications

Evidence for a Bacterial Lipopolysaccharide-Recognizing G-Protein-Coupled Receptor in the Bacterial Engulfment by Entamoeba histolytica

Evidence for a Bacterial Lipopolysaccharide-Recognizing G-Protein-Coupled Receptor in the Bacterial Engulfment by Entamoeba histolytica

Interactions between parasites and microbial communities in the human gut

Lectin–epithelial interactions in the human colon

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