scholarly journals Inhibitory effect of ecabet sodium on pepsin-induced degradation of rat gastric mucus gel layer in vitro

1997 ◽  
Vol 73 ◽  
pp. 78
Author(s):  
Mine Kinpshita ◽  
Mika Endo ◽  
Akira Yasoshima ◽  
Susumu Chishima ◽  
Kazuva Yamasaki ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Gastric Mucus ◽  
Ecabet Sodium ◽  
Gel Layer ◽  
Mucus Gel

scholarly journals Colonisation of the Colonic Mucus Gel Layer With Butyrogenic and Hydrogenotropic Bacteria in Health and Ulcerative Colitis

2020 ◽  
Author(s):  
Helen Earley ◽  
Grainne Lennon ◽  
Desmond Winter ◽  
Calvin Coffey ◽  
Ronan O'Connell
Keyword(s):  
Ulcerative Colitis ◽  
Inverse Correlation ◽  
Inhibitory Effect ◽  
Primary Energy ◽  
Rt Pcr ◽  
Mucosal Integrity ◽  
Gel Layer ◽  
Active Colitis ◽  
Mucus Gel ◽  
By Products

Abstract Butyrate is the primary energy source for colonocytes and is essential for mucosal integrity and repair. Butyrate deficiency as a result of colonic dysbiosis is a putative factor in ulcerative colitis (UC). Commensal microbes are butyrogenic, while others have an inhibitory effect, through hydrogenotropic activity. The aim of this study was to quantify butyrogenic and hydrogenotropic species and determine their relationship with inflammation within the colonic mucus gel layer (MGL).Mucosal brushings were obtained from 20 patients with active colitis (AC), 20 healthy controls (HC) and 14 with quiescent colitis (QUC). Abundance of each species was determined by RT-PCR. Inflammatory scores were available for each patient. Statistical analyses were performed using Mann-Whitney-U and Kruskall-Wallis tests.Butyrogenic R. hominis was more abundant in health than UC (p<0.005). Hydrogenotropic B. wadsworthia was reduced in AC compared to HC and QUC (p<0.005). An inverse correlation existed between inflammation and R. hominis (ρ -0.460, p >0.005) and B. wadsworthia (ρ -0.646, p >0.005). Other hydrogenotropic species did not widely colonise the MGL. These data support a role for butyrogenic and some species of hydrogenotropic bacteria in UC. Butyrate deficiency in UC may be related to reduced microbial production, rather than inhibition by microbial by-products.

scholarly journals Thinning of the Gastric Mucus Gel Layer in H Pylori Positive Subjects with Advancing Age

1997 ◽  
Vol 26 (suppl 3) ◽  
pp. P8-P8
Author(s):  
J Newton ◽  
N Jordan ◽  
G Williams ◽  
A Allen ◽  
O James ◽  
...  
Keyword(s):  
Gastric Mucus ◽  
Gel Layer ◽  
Mucus Gel ◽  
H Pylori

Use of Fluorescent Hydrophobic Dyes in Establishing the Presence of Lipids in the Gastric Mucus Gel Layer

1992 ◽  
Vol 14 ◽  
pp. S82-S87 ◽  
Author(s):  
Lenard M. Lichtenberger ◽  
Tariq N. Ahmed ◽  
José C. Barreto ◽  
Ya-Chu Judy Kao ◽  
Elizabeth J. Dial
Keyword(s):  
Gastric Mucus ◽  
Gel Layer ◽  
Mucus Gel

A new method of separation and quantitation of mucus glycoprotein in rat gastric mucus gel layer and its application to mucus secretion induced by 16,16-dimethyl PGE2

1991 ◽  
Vol 26 (5) ◽  
pp. 582-587 ◽  
Author(s):  
Yuichi Komuro ◽  
Kazuhiko Ishihara ◽  
Susumu Ohara ◽  
Katsunori Saigenji ◽  
Kyoko Hotta
Keyword(s):  
Mucus Secretion ◽  
New Method ◽  
Gastric Mucus ◽  
Mucus Glycoprotein ◽  
Gel Layer ◽  
Mucus Gel

Human spasmolytic polypeptide decreases proton permeation through gastric mucus in vivo and in vitro

1997 ◽  
Vol 272 (6) ◽  
pp. G1473-G1480 ◽  
Author(s):  
S. Tanaka ◽  
D. K. Podolsky ◽  
E. Engel ◽  
P. H. Guth ◽  
J. D. Kaunitz
Keyword(s):  
Blood Flow ◽  
Intracellular Ph ◽  
Ussing Chamber ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Gastric Mucus ◽  
Doppler Flowmetry ◽  
Mucus Gel

Exogenously administered trefoil peptides are gastroprotective in rat injury models. We hypothesized that trefoil-associated gastroprotection occurred by decreasing the rate of proton permeation through mucus. Gastric surface cell intracellular pH and mucus gel thickness were measured by in vivo microscopy. Gastric mucosal blood flow was measured by laser-Doppler flowmetry. The effect of human spasmolytic peptide (hSP) on H+ diffusion through 5% purified porcine mucin was measured using an Ussing chamber. Buffering action of mucin was measured by titration. In vivo, gastric mucosal blood flow and mucus gel thickness were not affected by any of the treatments. Topical hSP, but not intravenous hSP, decreased initial acidification rate and elevated the intracellular pH of gastric surface cells during luminal acid challenge. In in vitro studies, hSP dose dependently decreased the diffusion coefficient of H+ through 5% porcine mucin solution. hSP had no significant effect on the buffering action of mucin solutions. These data support our hypothesis that hSP interacts with gastric mucin in a manner that inhibits proton permeation through the mucus gel layer.

Barrier function of the gastric mucus gel

1995 ◽  
Vol 269 (6) ◽  
pp. G994-G999 ◽  
Author(s):  
E. Engel ◽  
P. H. Guth ◽  
Y. Nishizaki ◽  
J. D. Kaunitz
Keyword(s):  
Epithelial Cells ◽  
Theoretical Models ◽  
Gastric Epithelium ◽  
Gastric Mucus ◽  
Proton Diffusion ◽  
Unstirred Layers ◽  
Mucus Gel ◽  
Theoretical Considerations

The gastric epithelium is covered by a continuous layer of secreted mucus and bicarbonate. The function of this mucobicarbonate layer in terms of protecting the epithelial cells from luminal acid is controversial. Several studies conducted in vitro have shown that gastric mucus can slow proton diffusion and can enable the formation of a pH gradient across the mucobicarbonate layer. In our laboratory, simultaneous measurements of intracellular pH and the thickness of the mucus gel overlying gastric surface cells in vivo indicated that surface cell acidification rates and mucus gel thickness were inversely related. This suggests that the gastric mucobicarbonate layer delays proton permeation into gastric surface cells, enabling secreted bicarbonate to neutralize luminal acid. Several theoretical models, including the effects of mucus and bicarbonate secretion, convection, stirring, and lipids are offered as a possible explanation for the experimental observations. Lipid content and additional unstirred layers outside of the mucus gel are offered as possible explanations for the experimental observations. On the basis of the available data and theoretical considerations, we can conclude that all of these factors probably interact in an integrated manner to protect the gastric epithelial cells from damage due to luminal acid.

The adherent gastrointestinal mucus gel layer: thickness and physical state in vivo

2001 ◽  
Vol 280 (5) ◽  
pp. G922-G929 ◽  
Author(s):  
C. Atuma ◽  
V. Strugala ◽  
A. Allen ◽  
L. Holm
Keyword(s):  
In Vivo Model ◽  
Mucus Layer ◽  
Epithelial Surface ◽  
Continuous Increase ◽  
Gel Layer ◽  
Luminal Side ◽  
Before And After ◽  
Mucus Gel

Divergent results from in vitro studies on the thickness and appearance of the gastrointestinal mucus layer have previously been reported. With an in vivo model, we studied mucus gel thickness over time from stomach to colon. The gastrointestinal tissues of Inactin-anesthetized rats were mounted luminal side up for intravital microscopy. Mucus thickness was measured with a micropipette before and after mucus removal by suction. The mucus layer was translucent and continuous; it was thickest in the colon (∼830 μm) and thinnest in the jejunum (∼123 μm). On mucus removal, a continuous, firmly adherent mucus layer remained attached to the epithelial surface in the corpus (∼80 μm), antrum (∼154 μm), and colon (∼116 μm). In the small intestine, this layer was very thin (∼20 μm) or absent. After mucus removal, there was a continuous increase in mucus thickness with the highest rate in the colon and the lowest rate in the stomach. In conclusion, the adherent gastrointestinal mucus gel in vivo is continuous and can be divided into two layers: a loosely adherent layer removable by suction and a layer firmly attached to the mucosa.

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