Radiocontrast agent and intraductal pressure promote the progression of post-ERCP pancreatitis by regulating inflammatory response, cellular apoptosis, and tight junction integrity

Pancreatology ◽  
2021 ◽  
Author(s):  
Di Zhang ◽  
Xiaohua Man ◽  
Lei Li ◽  
Jian Tang ◽  
Feng Liu
Keyword(s):  
Inflammatory Response ◽  
Tight Junction ◽  
Radiocontrast Agent ◽  
Cellular Apoptosis

scholarly journals Impacts of Fructose on Intestinal Barrier Function, Inflammation and Microbiota in a Piglet Model

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3515
Author(s):  
Pingting Guo ◽  
Haichao Wang ◽  
Linbao Ji ◽  
Peixia Song ◽  
Xi Ma
Keyword(s):  
Inflammatory Response ◽  
Tight Junction ◽  
Growth Performance ◽  
Oxidant Stress ◽  
Intestinal Barrier ◽  
Sensu Stricto ◽  
Intestinal Barrier Function ◽  
Human Beings ◽  
Barrier Dysfunction ◽  
Gene Expressions

The metabolic disorder caused by excessive fructose intake was reported extensively and often accompanied by intestinal barrier dysfunction. And the rising dietary fructose was consumed at an early age of human. However, related researches were almost conducted in rodent models, while in the anatomy and physiology of gastrointestinal tract, pig is more similar to human beings than rodents. Hence, weaned piglets were chosen as the model animals in our study to investigate the fructose’s impacts on intestinal tight junction, inflammation response and microbiota structure of piglets. Herein, growth performance, inflammatory response, oxidation resistance and ileal and colonic microbiota of piglet were detected after 35-day fructose supplementation. Our results showed decreased tight junction gene expressions in piglets after fructose addition, with no obvious changes in the growth performance, antioxidant resistance and inflammatory response. Moreover, fructose supplementation differently modified the microbiota structures in ileum and colon. In ileum, the proportions of Streptococcus and Faecalibacterium were higher in Fru group (fructose supplementation). In colon, the proportions of Blautia and Clostridium sensu stricto 1 were higher in Fru group. All the results suggested that tight junction dysfunction might be an earlier fructose-induced event than inflammatory response and oxidant stress and that altered microbes in ileum and colon might be the potential candidates to alleviate fructose-induced intestinal permeability alteration.

scholarly journals Isoastragaloside I suppresses LPS-induced tight junction disruption and monocyte adhesion on bEnd.3 cells via an activating Nrf2 antioxidant defense system

RSC Advances ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 464-471 ◽  
Author(s):  
Hong-Li Li ◽  
Jin-Mei Jin ◽  
Chun Yang ◽  
Ping Wang ◽  
Fei Huang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Tight Junction ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Monocyte Adhesion ◽  
Defense System ◽  
System P ◽  
Tight Junction Disruption

ISOI rescued TJs disruption from ROS induced by LPS in bEnd.3 cells. ISOI ameliorated inflammatory response and decreased monocyte adhesion onto bEnd.3 cells induced with LPS. ISOI protected BBB integrity through activating Nrf2 antioxidant pathway.

scholarly journals Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3315
Author(s):  
Qiuyu Zhang ◽  
Lei Cheng ◽  
Junjuan Wang ◽  
Mengzhen Hao ◽  
Huilian Che
Keyword(s):  
Food Allergy ◽  
Inflammatory Response ◽  
Gut Microbiota ◽  
Tight Junction ◽  
Intestinal Barrier ◽  
Later Life ◽  
Food Allergies ◽  
Tight Junction Proteins ◽  
Gut Microbiota Dysbiosis ◽  
Junction Proteins

(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis’ impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.

scholarly journals Lactobacillus casei Zhang Counteracts Blood-Milk Barrier Disruption and Moderates the Inflammatory Response in Escherichia coli-Induced Mastitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuhui Zheng ◽  
Gang Liu ◽  
Wei Wang ◽  
Yajing Wang ◽  
Zhijun Cao ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Inflammatory Response ◽  
Tight Junction ◽  
Lactobacillus Casei ◽  
Mammary Tissue ◽  
Tight Junction Proteins ◽  
E Coli ◽  
Tnf Α ◽  
Injury Models ◽  
Junction Proteins

Escherichia coli is a common mastitis-causing pathogen that can disrupt the blood-milk barrier of mammals. Although Lactobacillus casei Zhang (LCZ) can alleviate mice mastitis, whether it has a prophylactic effect on E. coli-induced mastitis through intramammary infusion, as well as its underlying mechanism, remains unclear. In this study, E. coli-induced injury models of bovine mammary epithelial cells (BMECs) and mice in lactation were used to fill this research gap. In vitro tests of BMECs revealed that LCZ significantly inhibited the E. coli adhesion (p < 0.01); reduced the cell desmosome damage; increased the expression of the tight junction proteins claudin-1, claudin-4, occludin, and zonula occludens-1 (ZO-1; p < 0.01); and decreased the expression of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 (p < 0.01), thereby increasing trans-epithelial electric resistance (p < 0.01) and attenuating the lactate dehydrogenase release induced by E. coli (p < 0.01). In vivo tests indicated that LCZ significantly reduced the injury and histological score of mice mammary tissues in E. coli-induced mastitis (p < 0.01) by significantly promoting the expression of the tight junction proteins claudin-3, occludin, and ZO-1 (p < 0.01), which ameliorated blood-milk barrier disruption, and decreasing the expression of the inflammatory cytokines (TNF-α, IL-1β, and IL-6) in mice mammary tissue (p < 0.01). Our study suggested that LCZ counteracted the disrupted blood-milk barrier and moderated the inflammatory response in E. coli-induced injury models, indicating that LCZ can ameliorate the injury of mammary tissue in mastitis.

scholarly journals Zinc ameliorates intestinal barrier dysfunctions in shigellosis by reinstating claudin-2 and -4 on the membranes

2019 ◽  
Vol 316 (2) ◽  
pp. G229-G246 ◽  
Author(s):  
Paramita Sarkar ◽  
Tultul Saha ◽  
Irshad Ali Sheikh ◽  
Subhra Chakraborty ◽  
Joydeep Aoun ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Tight Junction ◽  
Barrier Function ◽  
Intracellular Signaling ◽  
Ion Selectivity ◽  
Intestinal Lumen ◽  
Mouse Tissue ◽  
Barrier Dysfunction ◽  
Intracellular Location ◽  
Junction Protein

Whether zinc (Zn2+) regulates barrier functions by modulating tight-junction (TJ) proteins when pathogens such as Shigella alter epithelial permeability is still unresolved. We investigated the potential benefits of Zn2+ in restoring impaired barrier function in vivo in Shigella-infected mouse tissue and in vitro in T84 cell monolayers. Basolateral Shigella infection triggered a time-dependent decrease in transepithelial resistance followed by an increase in paracellular permeability of FITC-labeled dextran and altered ion selectivity. This led to ion and water loss into the intestinal lumen. Immunofluorescence studies revealed redistribution of claudin-2 and -4 to an intracellular location and accumulation of these proteins in the cytoplasm following infection. Zn2+ ameliorated this perturbed barrier by redistribution of claudin-2 and -4 back to the plasma membrane and by modulating the phosphorylation state of TJ proteins t hough extracellular signal-regulated kinase (ERK)1/2 dependency. Zn2+ prevents elevation of IL-6 and IL-8. Mice challenged with Shigella showed that oral Zn2+supplementation diminished diverse pathophysiological symptoms of shigellosis. Claudin-2 and -4 were susceptible to Shigella infection, resulting in altered barrier function and increased levels of IL-6 and IL-8. Zn2+ supplementation ameliorated this barrier dysfunction, and the inflammatory response involving ERK-mediated change of phosphorylation status for claudin-2 and -4. Thus, Zn2+ may have potential therapeutic value in inflammatory diarrhea and shigellosis. NEW & NOTEWORTHY Our study addresses whether Zn2+ could be an alternative strategy to reduce Shigella-induced inflammatory response and epithelial barrier dysfunction. We have defined a mechanism in terms of intracellular signaling pathways and tight-junction protein expression by Zn2+. Claudin-2 and -4 are susceptible to Shigella infection, whereas in the presence of Zn2+ they are resistant to infection-related barrier dysfunction involving ERK-mediated change of phosphorylation status of claudins.

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