The gut microbiota metabolite propionate ameliorates intestinal epithelial barrier dysfunction-mediated Parkinson’s disease via the AKT signaling pathway

Neuroreport ◽  
2021 ◽  
Vol 32 (3) ◽  
pp. 244-251
Author(s):  
Tingting Huang ◽  
Hongjuan Shi ◽  
Yuanfeng Xu ◽  
Lili Ji
Keyword(s):  
Parkinson’S Disease ◽  
Gut Microbiota ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Akt Signaling Pathway ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Dysfunction

Flaxseed oligosaccharides alleviate DSS-induced colitis through modulation of gut microbiota and repair of the intestinal barrier in mice

2020 ◽  
Vol 11 (9) ◽  
pp. 8077-8088
Author(s):  
Zhenxia Xu ◽  
Wenchao Chen ◽  
Qianchun Deng ◽  
Qingde Huang ◽  
Xu Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Dysfunction

Intestinal epithelial barrier dysfunction with dysbiosis of gut microbiota contributes to the occurrence and acceleration of colitis.

Imbalance of gut microbiome and intestinal epithelial barrier dysfunction in cardiovascular disease

2018 ◽  
Vol 132 (8) ◽  
pp. 901-904 ◽  
Author(s):  
Judith N. Lezutekong ◽  
Anish Nikhanj ◽  
Gavin Y. Oudit
Keyword(s):  
Cardiovascular Disease ◽  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Epithelial Barrier ◽  
Main Function ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Physiological Homeostasis ◽  
Epithelial Barrier Dysfunction

The main function of the intestinal barrier is to regulate the absorption of nutrients, electrolytes, and water from the lumen into circulation and to prevent the entry of pathogenic microorganisms and toxic luminal substances. To maintain this function, an ideal microbiota balance is required and gut microbiota are critical for the intestinal epithelial barrier dysfunction and for the maintenance of physiological homeostasis. There is a demonstrable link between dysbiosis and intestinal dysfunction and diseases such as diabetes, obesity, and cardiovascular disease. However, links amongst gut pathology, microbial ecology, and blood pressure remain elusive. In a recent issue of Clinical Science (vol. 132, issue 6, 701-718), Kim et al. demonstrate a crucial link between gut microbiota and bacterial metabolites such as butyrate, gut leakiness, and hypertension.

scholarly journals Intestinal Epithelial Barrier Dysfunction in Food Hypersensitivity

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Linda Chia-Hui Yu
Keyword(s):  
Mast Cell ◽  
Cell Surface ◽  
Critical Role ◽  
Mast Cell Activation ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Food Antigens ◽  
Epithelial Barrier Dysfunction

Intestinal epithelial barrier plays a critical role in the maintenance of gut homeostasis by limiting the penetration of luminal bacteria and dietary allergens, yet allowing antigen sampling for the generation of tolerance. Undigested proteins normally do not gain access to the lamina propria due to physical exclusion by tight junctions at the cell-cell contact sites and intracellular degradation by lysosomal enzymes in enterocytes. An intriguing question then arises: how do macromolecular food antigens cross the epithelial barrier? This review discusses the epithelial barrier dysfunction in sensitized intestine with special emphasis on the molecular mechanism of the enhanced transcytotic rates of allergens. The sensitization phase of allergy is characterized by antigen-induced cross-linking of IgE bound to high affinity FcεRI on mast cell surface, leading to anaphylactic responses. Recent studies have demonstrated that prior to mast cell activation, food allergens are transported in large quantity across the epithelium and are protected from lysosomal degradation by binding to cell surface IgE and low-affinity receptor CD23/FcεRII. Improved immunotherapies are currently under study including anti-IgE and anti-CD23 antibodies for the management of atopic disorders.

scholarly journals Homocysteine Aggravates Intestinal Epithelial Barrier Dysfunction in Rats with Experimental Uremia

2018 ◽  
Vol 43 (5) ◽  
pp. 1516-1528 ◽  
Author(s):  
Shanshan Liang ◽  
Sixiu Liu ◽  
Hua Liu ◽  
Xin He ◽  
Lingshuang Sun ◽  
...  
Keyword(s):  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Dysfunction

scholarly journals Chymase-mediated intestinal epithelial permeability is regulated by a protease-activating receptor/matrix metalloproteinase-2-dependent mechanism

2013 ◽  
Vol 304 (5) ◽  
pp. G479-G489 ◽  
Author(s):  
Katherine R. Groschwitz ◽  
David Wu ◽  
Heather Osterfeld ◽  
Richard Ahrens ◽  
Simon P. Hogan
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Epithelial Barrier Dysfunction

Mast cells regulate intestinal barrier function during disease and homeostasis. Secretion of the mast cell-specific serine protease chymase regulates homeostasis. In the present study, we employ in vitro model systems to delineate the molecular pathways involved in chymase-mediated intestinal epithelial barrier dysfunction. Chymase stimulation of intestinal epithelial (Caco-2 BBe) cell monolayers induced a significant reduction in transepithelial resistance, indicating decreased intestinal epithelial barrier function. The chymase-induced intestinal epithelial barrier dysfunction was characterized by chymase-induced protease-activated receptor (PAR)-2 activation and matrix metalloproteinase (MMP)-2 expression and activation. Consistent with this observation, in vitro analysis revealed chymase-induced PAR-2 activation and increased MAPK activity and MMP-2 expression. Pharmacological and small interfering RNA-mediated antagonism of PAR-2 and MMP-2 significantly attenuated chymase-stimulated barrier dysfunction. Additionally, the chymase/MMP-2-mediated intestinal epithelial dysfunction was associated with a significant reduction in the tight junction protein claudin-5, which was partially restored by MMP-2 inhibition. Finally, incubation of Caco-2 BBe cells with chymase-sufficient, but not chymase-deficient, bone marrow-derived mast cells decreased barrier function, which was attenuated by the chymase inhibitor chymostatin. Collectively, these results suggest that mast cell/chymase-mediated intestinal epithelial barrier function is mediated by PAR-2/MMP-2-dependent pathways.

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