The Gastric Mucosal Barrier

Hirst, Barry H.

doi:10.1002/cphy.cp060315

Cited by 11 publications

(8 citation statements)

References 183 publications

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“…The absence of a local inflammatory response in the stomach of these rats suggests that the loss of tight junction apposition was not sufficient to allow pathogens through the mucosal barrier to cause serious damage of underlying tissue and consequently trigger a local inflammatory response [56]. The permeability of the mucosal barrier is also determined by the presence of the basement membrane (which acts as a selective chemical barrier) and the mucous layer protecting the mucosal surface of the stomach [57]. Therefore any organism or substance would have to also breach these barrier components [58].…”

Section: Tight Junction Apposition Lossmentioning

confidence: 99%

“…Alternatively, elongation of epithelial cells in the gut mucosa could reflect a rapid repair mechanism called restitution, which occurs following an insult to the mucosal surface epithelium [57]. The mechanism involves the elongation of the remaining viable cells to cover the basal lamina to maintain mucosal barrier integrity and continuity until other mechanisms ensue, such as cellular proliferation and/or an extensive inflammatory response [58].…”

Section: Other Observed Changesmentioning

confidence: 99%

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Histopathological Investigation of the Stomach of Rats Fed a 60% Genetically Modified Corn Diet

Zdziarski¹,

Carman²,

Edwards³

2018

FNS

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Genetic modification (GM) represents new opportunities for enhanced crop features such as improved insect resistance and herbicide tolerance. The technology allows for cross-species alterations, therefore potentially allowing a vast array of novel traits. Many GM crops have been developed and approved for human and animal consumption. The present study investigated a triple-stacked GM corn variety containing modifications for insect resistance (via cry1Ab and cry3Bb1 genes) and herbicide tolerance (via an EPSPS gene), which was fed to rats for six months. The study investigated the mucosa of the stomach. Alterations to tight junction apposition, gland dilatations with epithelial elongation and dysplasia in the GM-fed rats were observed. These results indicate that GM-corn may have an effect on rat stomach mucosa, which may have health implications.

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Section: Tight Junction Apposition Lossmentioning

confidence: 99%

Section: Other Observed Changesmentioning

confidence: 99%

Histopathological Investigation of the Stomach of Rats Fed a 60% Genetically Modified Corn Diet

Zdziarski¹,

Carman²,

Edwards³

2018

FNS

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“…'819 In the present study we have investigated whether prostaglandin E, (PGE2) has a direct protective action on upper gastrointestinal luminal membranes by studying their ability to reduce the increase in proton permeability induced by bile salts in rabbit duodenal brush border membrane vesicles. 6 5 solution (150 mmol/l K' gluconate, 10 mmol/l hydroxyethylpiperazine-ethanesulphonic acid (HEPES)/Tris) containing 4 ,umol/l valinomycin (to voltage-clamp the vesicles), with varying concentrations of bile salts or PGE2, or both. Proton permeation was monitored by diluting vesicles in 150 mmol/l K' gluconate, 6 ,umol/l acridine orange, 10 mmol/l HEPES/Tris at pH 8 Deoxycholate, glycodeoxycholate, and taurodeoxycholate acid (Steraloids) and PGE2 (Sigma) were made up fresh each day and final pH adjusted after sonication.…”

mentioning

confidence: 99%

Prostaglandin protects against bile salt induced increases in proton permeation of duodenal brush border membrane.

Zhao

Hirst

1991

Gut

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A direct protective action of prostaglandin on luminal cell membranes was investigated by preincubating rabbit duodenal brush border membrane vesicles with prostaglandin E, (PGE,) before incubation with bile salts. Membrane perturbation was assessed by measuring the net proton permeability (P.,).Bile salts (deoxycholate, glycodeoxycholate, and taurodeoxycholate; 041-1.0 mmol/l) resulted in concentration dependent increases in P.,: from (mean (SE)) 5.42 (0.17) (n=20) to 8.44 (0.24)x10-4 (n=13) cm/s with 0.5 mmol/l deoxycholate. PGE2, 1-810-6 mol/, when added alone had no effect on P..,: 5-41 (0.21) X10-4 (n=14) cm/s with 10-' M PGE2. When duodenal brush border membranes were preincubated with PGE2, 10-'-10-' moll, however, the bile salt induced increase in Pnet was significantly reduced: 7-22 (0.18)x 104 (n= 13) cm/s with 10-' mol/l PGE2 and 0.5 mmol/l deoxycholate. These findings indicate that PGE2 exerts a direct protective action on duodenal luminal membranes.

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“…The fundic mucosa is characterized as an electrically tight epithelium, and as part of its normal function resists the backdiffusion of H+ from the lumen into the tissue. This functional barrier is provided by the apical membranes of the epithelial cells of the gastric mucosa and the intercellular tight junctions (Hirst, 1989(Hirst, , 1990. In gastric epithelia, increasing luminal acidity is associated with an increase in transmucosal electrical resistance, i.e.…”

Section: Introductionmentioning

confidence: 99%

Transmucosal electrical resistance in rabbit isolated gastric mucosa during exposure to acid.

Spencer

Spraggs

Stables

et al. 1992

The Journal of Physiology

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SUMMARY1. Transmucosal electrical resistance (Rj) and short-circuit current (1S,) were determined in rabbit isolated fundic mucosa. Under basal conditions, with a HCO3--free HEPES-buffered solution (pH 7 4) bathing both sides of the mucosae, Rt was 161-5 + 5-0 Q cm2 and I_C 41 8 + 1P8 ,tA cm-2, and these values were not significantly different to values observed in HC03--buffered Krebs-Hensleit solution.2. The basal 'SC was inhibited by the Cl-channel blocker diphenylamine-2-carboxylate, and ouabain, but unaffected by the Na+ channel blocker amiloride (10-M), consistent with electrogenic chloride secretion dependent upon a sodium gradient. Prostaglandin E2 (10-7 M) stimulated an increase in ISC which was susceptible to inhibition by diphenylamine-2-carboxylate, but not amiloride, again consistent with Cl-secretion.3. Stepwise acidification of the mucosal solution to pH 2-8 resulted in an increase in Rt of 43%, as compared with that measured with mucosal pH 7-4. IC did not change during the acidification to pH 2-8, indicating retention of tissue viability. Increased Rt while IS remained constant is consistent with an acid-induced decrease in the shunt (paracellular) conductance in this Cl--secreting tissue. At pH < 2-8, Rt declined rapidly and ISC declined and reversed, consistent with H' back-diffusion.

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The Gastric Mucosal Barrier

Cited by 11 publications

References 183 publications

Histopathological Investigation of the Stomach of Rats Fed a 60% Genetically Modified Corn Diet

Histopathological Investigation of the Stomach of Rats Fed a 60% Genetically Modified Corn Diet

Prostaglandin protects against bile salt induced increases in proton permeation of duodenal brush border membrane.

Transmucosal electrical resistance in rabbit isolated gastric mucosa during exposure to acid.

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