Binding of proteolytically-degraded human colonic mucin glycoproteins to the Gal/GalNAc adherence lectin of Entamoeba histolytica.

Chadee, Kris; Ndarathi, C.M.; Keller, Kathy

doi:10.1136/gut.31.8.890

Cited by 18 publications

(6 citation statements)

References 27 publications

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“…Bar is equal to 730 nm GC GC a b Fig. 3 Transmission electronic microphotography shows the intact brush border (arrows) and tight junctions (curved arrows): a individualized mucine granules in a goblet cell, b a goblet cell in the discharge process (GC) in a potentially similar way as that observed in amoeba (Chadee et al 1990), thus impairing the adherence of Giardia to epithelial cells or, alternatively, as observed for Nippostrongylus brasiliensis (Ishikawa et al 1993), via modification of the terminal sugar of the mucin. So far, information on this subject appears to be contradictory, since there is at least one work supporting the beneficial effect of human mucus on Giardia growth, while other observations (Roskens and Erlandsen 2002) show the opposite effect, as reviewed by Müller and von Allmen (2005).…”

Section: Discussionmentioning

confidence: 85%

“…The unspecific responses are partially supported by nitric oxide, antimicrobial peptides, and others (Eckmann 2003) as well as the mucus-secreting goblet cells (GC) that protect the gut by layering the epithelium (Ho et al 1995). There are supporting evidences showing that mucus glycoproteins act by inhibiting the adherence of Escherichia coli (Mack and Sherman 1991) and Entamoeba histolytica (Chadee et al 1990) to epithelial cells. In addition, there are data showing that some compounds present in the secretion of goblet cells impede rotaviruses' replication (Yolken et al 1994).…”

Section: Introductionmentioning

confidence: 99%

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Goblet cells: are they an unspecific barrier against Giardia intestinalis or a gate?

et al. 2007

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Giardiosis is one of the major intestinal parasitic diseases of human beings as well as wild and domesticated animals. Several protective mechanisms against infection have been described. However, specific information about relationship between giardiosis and the increased proliferation of goblet cells (GC) in patients infected with Giardia intestinalis (Syn. G. duodenalis, G. lamblia) is scarce. In this work, we compare and quantify the number of GC, and have inferred their metabolic state in the small intestine of dogs parasitized with Giardia intestinalis compared to dogs without parasites. Small intestine segments were processed using routine methods for histology and electron microscopy; areas and cells were screened with an Axiovision Ver. 4.0 system. Data were analyzed by ANOVA and comparison of averages. Parasitized dogs showed higher GC numbers than nonparasitized ones. Averages were: 20+/-0.81 GC/25 microm(2) with independent mucin granules and 11+/-1.53 GC/25 microm(2) that were expelling mucus, compared to 11+/-0.94 GC/25 microm(2) and 1+/-0.27 GC/25 microm(2), respectively, in nonparasitized dogs (Tukey, p<0.001). The increases in GC number seem to be an unspecific defensive mechanism against Giardia trophozoites. However, we found some evidence supporting that GC hyperplasia could be a prejudicial to epithelial barrier that gives rise to gates allowing for Giardia-tissue invasion.

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Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Goblet cells: are they an unspecific barrier against Giardia intestinalis or a gate?

et al. 2007

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“…Although the inflammatory response produced in the above-mentioned SCID-HU-INT mouse model partially reproduces the early steps of human intestinal parasite invasion, this model lacks lymphocyte responses [17] and it does not take into account the role of the human colonic mucus. Among E. histolytica components Gal/GalNAc lectin is a major factor for adherence to mucus [18] and epithelial cells. It has been reported Gal-GalNAc lectin-mediated contact between trophozoites and human epithelial cells and leukocytes induces cell apoptosis [19] .…”

Section: Introductionmentioning

confidence: 99%

An ex-vivo Human Intestinal Model to Study Entamoeba histolytica Pathogenesis

et al. 2009

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Amoebiasis (a human intestinal infection affecting 50 million people every year) is caused by the protozoan parasite Entamoeba histolytica. To study the molecular mechanisms underlying human colon invasion by E. histolytica, we have set up an ex vivo human colon model to study the early steps in amoebiasis. Using scanning electron microscopy and histological analyses, we have established that E. histolytica caused the removal of the protective mucus coat during the first two hours of incubation, detached the enterocytes, and then penetrated into the lamina propria by following the crypts of Lieberkühn. Significant cell lysis (determined by the release of lactodehydrogenase) and inflammation (marked by the secretion of pro-inflammatory molecules such as interleukin 1 beta, interferon gamma, interleukin 6, interleukin 8 and tumour necrosis factor) were detected after four hours of incubation. Entamoeba dispar (a closely related non-pathogenic amoeba that also colonizes the human colon) was unable to invade colonic mucosa, lyse cells or induce an inflammatory response. We also examined the behaviour of trophozoites in which genes coding for known virulent factors (such as amoebapores, the Gal/GalNAc lectin and the cysteine protease 5 (CP-A5), which have major roles in cell death, adhesion (to target cells or mucus) and mucus degradation, respectively) were silenced, together with the corresponding tissue responses. Our data revealed that the signalling via the heavy chain Hgl2 or via the light chain Lgl1 of the Gal/GalNAc lectin is not essential to penetrate the human colonic mucosa. In addition, our study demonstrates that E. histolytica silenced for CP-A5 does not penetrate the colonic lamina propria and does not induce the host's pro-inflammatory cytokine secretion.

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“…In vitro labelling of colonic glycoproteins with NaB[3H14. In parallel experiments, secreted unlabelled colonic glycopro-teins were harvested from PBS-, CT-, and E. histolyticaexposed loops and labelled in vitro by sodium metaperiodate oxidation treatment (Sigma Chemical Co.) followed by reduction with NaB[3H]4 as previously described (9,29). Crude mucus (100 to 200 ,ug) was suspended in 0.5 to 1.0 ml of PBS (pH 7.4) containing 10 mM sodium metaperiodate and incubated in the dark (0°C) for 1 h. Excess periodate was removed from the samples by dialyzing against PBS (12,000to 14,000-Mr exclusion) for 12 h. The nondialyzable material then underwent reduction treatment by addition of 5 mCi of NaB3H4 (specific activity, >100 mCi/mmol; NEN, Mississauga, Ontario, Canada) at 37°C for 35 min.…”

Section: Methodsmentioning

confidence: 99%

Biochemical characterization of rat colonic mucins secreted in response to Entamoeba histolytica

Tse

Chadee

1992

Infect Immun

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Invasion of the colonic mucosa by Entamoeba histolytica trophozoites is preceded by colonic mucus depletion. The aim of our studies was to determine whether E. histolytica caused a differential secretion of mucin species in a rat colonic loop model. Mucus secretion in response to amoebae was followed by release of acid-precipitable 3H-glucosamine metabolically labelled glycoproteins and in vitro labelling of glycoprotein secretion with NaB3H4. The secretory response consisted of high-Mr goblet cell mucins and an increase in the secretion of low-Mr nonmucin glycoproteins as determined by Sepharose 4B column chromatography. High-Mr mucins subfractionated by Cellex-E (ECTEOLA) ion-exchange chromatography demonstrated a minor neutral and a major acidic mucin (greater than 98%) species. Marked differences between the neutral and acidic mucin species were indicated by immunogenicity and amino acid compositions. Thin-section histochemistry of rat colons confirmed secretion of neutral and acidic mucins in response to E. histolytica and demonstrated secretory activity from goblet cells from both the crypts and interglandular epithelium. E. histolytica mucus secretagogue activity was generalized and may function to deplete the host's protective mucus layer, facilitating invasion by the parasites.

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Binding of proteolytically-degraded human colonic mucin glycoproteins to the Gal/GalNAc adherence lectin of Entamoeba histolytica.

Cited by 18 publications

References 27 publications

Goblet cells: are they an unspecific barrier against Giardia intestinalis or a gate?

Goblet cells: are they an unspecific barrier against Giardia intestinalis or a gate?

An ex-vivo Human Intestinal Model to Study Entamoeba histolytica Pathogenesis

Biochemical characterization of rat colonic mucins secreted in response to Entamoeba histolytica

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