The Vat-AIEC protease promotes crossing of the intestinal mucus layer by Crohn's disease-associatedEscherichia coli

2015 ◽  
Vol 18 (5) ◽  
pp. 617-631 ◽  
Author(s):  
Lucie Gibold ◽  
Estelle Garenaux ◽  
Guillaume Dalmasso ◽  
Camille Gallucci ◽  
David Cia ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Mucus Layer ◽  
Intestinal Mucus ◽  
Intestinal Mucus Layer

scholarly journals Oxyresveratrol Ameliorates Dextran Sulfate Sodium-Induced Colitis in Rats by Suppressing Inflammation

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2630
Author(s):  
Jiah Yeom ◽  
Seongho Ma ◽  
Jeong-Keun Kim ◽  
Young-Hee Lim
Keyword(s):  
Inflammatory Cytokine ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Mucus Layer ◽  
Beneficial Effects ◽  
Intestinal Mucus ◽  
Anti Inflammatory ◽  
Apoptotic Effects ◽  
Intestinal Mucus Layer

Colitis causes destruction of the intestinal mucus layer and increases intestinal inflammation. The use of antioxidants and anti-inflammatory agents derived from natural sources has been recently highlighted as a new approach for the treatment of colitis. Oxyresveratrol (OXY) is an antioxidant known to have various beneficial effects on human health, such as anti-inflammatory, antibacterial activity, and antiviral activity. The aim of this study was to investigate the therapeutic effect of OXY in rats with dextran sulfate sodium (DSS)-induced acute colitis. OXY ameliorated DSS-induced colitis and repaired damaged intestinal mucosa. OXY downregulated the expression of pro-inflammatory cytokine genes (TNF-α, IL-6, and IL-1β) and chemokine gene MCP-1, while promoting the production of anti-inflammatory cytokine IL-10. OXY treatment also suppressed inflammation via inhibiting cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression in the colon, as well as the activity of myeloperoxidase (MPO). OXY exhibited anti-apoptotic effects, shifting the Bax/Bcl-2 balance. In conclusion, OXY might improve DSS-induced colitis by restoring the intestinal mucus layer and reducing inflammation within the intestine.

Improvement of a ‘Leaky' Intestinal Barrier

2017 ◽  
Vol 35 (1-2) ◽  
pp. 21-24 ◽  
Author(s):  
Eduard F. Stange
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Intestinal Barrier ◽  
Bacterial Attachment ◽  
Phase Iii ◽  
Colonic Disease ◽  
Mucus Layer ◽  
Tissue Destruction ◽  
Liquid Form ◽  
Mucus Production

In Crohn's disease, the mucus layer appears to be defective in terms of low defensin levels and lack of antibacterial activity. These deficiencies actually explain the Montreal phenotypes and the stable localization of disease in the terminal ileum with low α-defensins from Paneth cells and/or low β-defensins in colonic disease, respectively. Conversely, in ulcerative colitis (UC) the defensin production is normal or even induced, but the mucus layer is thinner and patchy, more in the liquid form and also chemically altered so that antibacterial peptides are not retained and lost into the luminal bacterial bulk. Therefore, both barrier problems allow slow bacterial attachment and invasion, ultimately triggering the massive response of adaptive immunity and tissue destruction. Therefore, leakiness should refer to the antibacterial barrier and not to the general barrier against small molecules, such as mannitol or lactulose, which are not antigenic. The most promising approach in UC seems to be the use of probiotics or the natural compound lecithin as a stabilizer of mucus structure to enhance the barrier. While a phase II study has yielded positive results, the results of the ongoing phase III study are eagerly awaited. It is quite possible that the protective effect of smoking in UC is related to mucus production in the colon also, but this is not an option. Another alternative would be to shift cell differentiation in the colon towards goblet cell; the relevant differentiation factors are known. In Crohn's disease, the direct oral application of defensins might be effective if release and binding to the mucus are achieved. In the experimental colitis model, this works quite well. In conclusion, in a situation where enthusiasm about so-called biologics is declining due to loss of response over time, searching for the primary defects in inflammatory bowel disease and treating them may well be worthwhile, although it is unlikely to provide rapid relief.

scholarly journals In Vitro Reconstitution of an Intestinal Mucus Layer Shows That Cations and pH Control the Pore Structure That Regulates Its Permeability and Barrier Function

2020 ◽  
Vol 3 (5) ◽  
pp. 2897-2909 ◽  
Author(s):  
Abhinav Sharma ◽  
Jun-Goo Kwak ◽  
Kristopher W. Kolewe ◽  
Jessica D. Schiffman ◽  
Neil S. Forbes ◽  
...  
Keyword(s):  
Pore Structure ◽  
Barrier Function ◽  
Ph Control ◽  
Mucus Layer ◽  
Intestinal Mucus ◽  
In Vitro Reconstitution ◽  
Intestinal Mucus Layer

scholarly journals Intestinal Mucus Layer Preservation in Female Rats Attenuates Gut Injury After Trauma-Hemorrhagic Shock

2010 ◽  
Vol 68 (2) ◽  
pp. 279-288 ◽  
Author(s):  
Sharvil U. Sheth ◽  
Qi Lu ◽  
Kate Twelker ◽  
Susan M. Sharpe ◽  
Xiaofa Qin ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Female Rats ◽  
Mucus Layer ◽  
Intestinal Mucus ◽  
Intestinal Mucus Layer

scholarly journals The fate of cellulose nanocrystal stabilised emulsions after simulated gastrointestinal digestion and exposure to intestinal mucosa

Nanoscale ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 2991-2998 ◽  
Author(s):  
Alan Mackie ◽  
Simon Gourcy ◽  
Neil Rigby ◽  
Jonathan Moffat ◽  
Isabel Capron ◽  
...  
Keyword(s):  
Intestinal Mucosa ◽  
Cellulose Nanocrystals ◽  
Cellulose Nanocrystal ◽  
Mucus Layer ◽  
Gastrointestinal Digestion ◽  
Simulated Gastrointestinal Digestion ◽  
Intestinal Mucus ◽  
Intestinal Mucus Layer

The intestinal mucus layer prevents cellulose nanocrystals from reaching the epithelium and can modulate lipid and bile absorption.

The Intestinal Mucus Layer Comes of Age

2016 ◽  
Vol 37 (1) ◽  
pp. 3-4 ◽  
Author(s):  
Shipra Vaishnava
Keyword(s):  
Mucus Layer ◽  
Intestinal Mucus ◽  
Intestinal Mucus Layer

scholarly journals Bifidobacterium dentiumFortifies the Intestinal Mucus Layer via Autophagy and Calcium Signaling Pathways

mBio ◽  
2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Melinda A. Engevik ◽  
Berkley Luk ◽  
Alexandra L. Chang-Graham ◽  
Anne Hall ◽  
Beatrice Herrmann ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Signaling Pathways ◽  
Goblet Cell ◽  
Cell Function ◽  
Goblet Cells ◽  
Mucus Layer ◽  
Content Type ◽  
Intestinal Mucus ◽  
Intestinal Mucus Layer

ABSTRACTMuch remains unknown about how the intestinal microbiome interfaces with the protective intestinal mucus layer.Bifidobacteriumspecies colonize the intestinal mucus layer and can modulate mucus production by goblet cells. However, selectBifidobacteriumstrains can also degrade protective glycans on mucin proteins. We hypothesized that the human-derived speciesBifidobacterium dentiumwould increase intestinal mucus synthesis and expulsion, without extensive degradation of mucin glycans.In silicodata revealed thatB. dentiumlacked the enzymes necessary to extensively degrade mucin glycans. This finding was confirmed by demonstrating thatB. dentiumcould not use naive mucin glycans as primary carbon sourcesin vitro. To examineB. dentiummucus modulationin vivo, Swiss Webster germfree mice were monoassociated with live or heat-killedB. dentium. LiveB. dentium-monoassociated mice exhibited increased colonic expression of goblet cell markersKrüppel-like factor 4(Klf4),Trefoil factor 3(Tff3),Relm-β,Muc2, and several glycosyltransferases compared to both heat-killedB. dentiumand germfree counterparts. Likewise, liveB. dentium-monoassociated colon had increased acidic mucin-filled goblet cells, as denoted by Periodic Acid-Schiff-Alcian Blue (PAS-AB) staining and MUC2 immunostaining.In vitro,B. dentium-secreted products, including acetate, were able to increase MUC2 levels in T84 cells. We also identified thatB. dentium-secreted products, such as γ-aminobutyric acid (GABA), stimulated autophagy-mediated calcium signaling and MUC2 release. This work illustrates thatB. dentiumis capable of enhancing the intestinal mucus layer and goblet cell function via upregulation of gene expression and autophagy signaling pathways, with a net increase in mucin production.IMPORTANCEMicrobe-host interactions in the intestine occur along the mucus-covered epithelium. In the gastrointestinal tract, mucus is composed of glycan-covered proteins, or mucins, which are secreted by goblet cells to form a protective gel-like structure above the epithelium. Low levels of mucin or alterations in mucin glycans are associated with inflammation and colitis in mice and humans. Although current literature links microbes to the modulation of goblet cells and mucins, the molecular pathways involved are not yet fully understood. Using a combination of gnotobiotic mice and mucus-secreting cell lines, we have identified a human-derived microbe,Bifidobacterium dentium, which adheres to intestinal mucus and secretes metabolites that upregulate the major mucin MUC2 and modulate goblet cell function. Unlike otherBifidobacteriumspecies,B. dentiumdoes not extensively degrade mucin glycans and cannot grow on mucin alone. This work points to the potential of usingB. dentiumand similar mucin-friendly microbes as therapeutic agents for intestinal disorders with disruptions in the mucus barrier.

OC.07.6 GELENTERUM AMELIORATES SEVERITY OF COLITIS IN DSS MURINE MODEL, WHILE MODULATING GUT MICROBIOTA AND INTESTINAL MUCUS LAYER

2013 ◽  
Vol 45 ◽  
pp. S72-S73
Author(s):  
F. Scaldaferri ◽  
L.R. Lopetuso ◽  
V. Petito ◽  
V. Gerardi ◽  
M. Bilotta ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Murine Model ◽  
Mucus Layer ◽  
Intestinal Mucus ◽  
Intestinal Mucus Layer
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