The mucus and bicarbonate barrier in gastroduodenal defence

Allen, Adrian; Garner, A.

doi:10.1007/978-1-349-17615-1_53

Cited by 5 publications

(4 citation statements)

References 40 publications

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“…H. pylori is a highly motile organism whose spiral progression is hypothesized to allow penetration of the mucus barrier to facilitate the intimate attachment at the gastric mucosal cell surface (12). The pH at the gastric mucosal surface is, however, neutral (1). It is therefore likely that once this location is achieved (except at erosion sites?…”

Section: Discussionmentioning

confidence: 99%

Acidic pH changes receptor binding specificity of Helicobacter pylori: a binary adhesion model in which surface heat shock (stress) proteins mediate sulfatide recognition in gastric colonization

et al. 1996

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The gastric pathogen Helicobacter pylori is one of a number of bacteria which bind specifically to gangliotetraosylceramide, gangliotriaosylceramide, and phosphatidylethanolamine in vitro at neutral pH. Since this organism encounters an acid pH during initial infection of the stomach, we have monitored the effect of pH on receptor binding specificity and found induction of specific binding to sulfoglycolipids (sulfatide) following brief treatment at low pH. We have previously shown that heat shock proteins (hsps) bind to sulfatide, and the suspicion that this was a stress-induced response is supported by the fact that a similar change in H. pylori binding specificity was observed if the organisms were briefly exposed to heat shock treatment. Following the stress stimulus, the change in glycolipid binding specificity was prevented by the inclusion of inhibitors of protein synthesis or by incubation with anti-hsp antibodies. Expression of hsps in the surface extract and surface reactivity with anti-hsp antibodies correlated with the change in glycolipid binding specificity. Despite the presence of high levels of H. pylori cell surface urease activity, which may neutralize the microenvironmental pH, the acid-induced change in binding specificity was enhanced in the presence of urea. These studies suggest that cell surface hsps mediate sulfatide recognition by this organism under stress conditions. A binary receptor model is proposed for gastric colonization by H. pylori.

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Section: Discussionmentioning

confidence: 99%

Acidic pH changes receptor binding specificity of Helicobacter pylori: a binary adhesion model in which surface heat shock (stress) proteins mediate sulfatide recognition in gastric colonization

et al. 1996

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“…The hydrochloric acid in the mammalian stomach is concentrated enough (pH 1–2) to digest the stomach [ 1 ], a finding made by René Antoine Ferchault de Réaumur in the eighteenth century [ 2 ]. However the epithelial lining of the stomach remains intact during the digestive process despite the potency of the acid, pepsin and shear associated with digestion [ 3 , 4 ], behaving, according to Claude Bernard, as if the stomach was made of porcelain [ 2 ]!…”

Section: Introductionmentioning

confidence: 99%

“…In 1959 Heatley [ 5 ] proposed that mucus on the gastric mucosal surface acted as a mixing barrier and postulated the existence of a pH gradient from the lumen (acid) to the mucosal surface (neutrality). This barrier, later known as the mucus-bicarbonate barrier [ 3 , 6 ] allowed a restricted mixing of hydrogen and bicarbonate ions [ 6 ], in a stable unstirred layer of variable thickness in humans between 50 and 540 μm (mean 180 μm) [ 7 ]. The epithelial surfaces of the major internal tracts of the body are protected by a continuous layer of crude mucus gel.…”

Section: Introductionmentioning

confidence: 99%

“…The gastric gel is readily permeable to both H + and HCO 3 − and provides an unstirred layer on the mucosal surface in which the HCO 3 − is secreted by the epithelial cells and is prevented from mixing with the bulk of the acid. Luminal acid is therefore neutralised before it reaches the mucosal cells [ 3 ]. Whilst permeable to low molecular weight solutes [ 32 ], the gel is impermeable to larger molecules such as pepsin, microbes [ 33 ] and certain viruses such as human papilloma virus and Merkel cell polyomavirus which are prevented from reaching the underlying epithelial cells [ 34 ].…”

Section: Introductionmentioning

confidence: 99%

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Mucus and Mucins: do they have a role in the inhibition of the human immunodeficiency virus?

Mall

Habte

Mthembu

et al. 2017

Virol J

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BackgroundMucins are large O-linked glycosylated proteins which give mucus their gel-forming properties. There are indications that mucus and mucins in saliva, breast milk and in the cervical plug inhibit the human immunodeficiency virus (HIV-1) in an in vitro assay.Main body of abstractCrude mucus gels form continuous layers on the epithelial surfaces of the major internal tracts of the body and protect these epithelial surfaces against aggressive luminal factors such as hydrochloric acid and pepsin proteolysis in the stomach lumen, the movement of hard faecal pellets in the colon at high pressure, the effects of shear against the vaginal epithelium during intercourse and the presence of foreign substances in the respiratory airways. Tumour-associated epitopes on mucins make them suitable as immune-targets on malignant epithelial cells, rendering mucins important as diagnostic and prognostic markers for various diseases, even influencing the design of mucin-based vaccines.Sub-Saharan Africa has the highest prevalence of HIV-AIDS in the world. The main points of viral transmission are via the vaginal epithelium during sexual intercourse and mother-to-child transmission during breast-feeding. There have been many studies showing that several body fluids have components that prevent the transmission of HIV-1 from infected to non-infected persons through various forms of contact.Crude saliva and its purified mucins, MUC5B and MUC7, and the purified mucins from breast milk, MUC1 and MUC4 and pregnancy plug cervical mucus (MUC2, MUC5AC, MUC5B and MUC6), inhibit HIV-1 in an in vitro assay. There are conflicting reports of whether crude breast-milk inhibits HIV-1 in an in vitro assay. However studies with a humanised BLT mouse show that breast-milk does inhibit HIV and that breast-feeding is still advisable even amongst HIV-positive women in under-resourced areas, preferably in conjunction with anti-retroviral treatment.ConclusionThese findings raise questions of how such a naturally occurring biological substance such as mucus, with remarkable protective properties of epithelial surfaces against aggressive luminal factors in delicate locations, could be used as a tool in the fight against HIV-AIDS, which has reached epidemic proportions in sub-Saharan Africa.

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