scholarly journals The Effect of Butyrate-Supplemented Parenteral Nutrition on Intestinal Defence Mechanisms and the Parenteral Nutrition-Induced Shift in the Gut Microbiota in the Rat Model

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Zuzana Jirsova ◽  
Marie Heczkova ◽  
Helena Dankova ◽  
Hana Malinska ◽  
Petra Videnska ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Parenteral Nutrition ◽  
Antimicrobial Peptides ◽  
Tight Junction ◽  
Microbiota Composition ◽  
Tight Junction Proteins ◽  
Defence Mechanisms ◽  
Altered Expression ◽  
Intestinal Immune System ◽  
Junction Proteins

Butyrate produced by the intestinal microbiota is essential for proper functioning of the intestinal immune system. Total dependence on parenteral nutrition (PN) is associated with numerous adverse effects, including severe microbial dysbiosis and loss of important butyrate producers. We hypothesised that a lack of butyrate produced by the gut microbiota may be compensated by its supplementation in PN mixtures. We tested whetheri.v.butyrate administration would (a) positively modulate intestinal defence mechanisms and (b) counteract PN-induced dysbiosis. Male Wistar rats were randomised to chow, PN, and PN supplemented with 9 mM butyrate (PN+But) for 12 days. Antimicrobial peptides, mucins, tight junction proteins, and cytokine expression were assessed by RT-qPCR. T-cell subpopulations in mesenteric lymph nodes (MLN) were analysed by flow cytometry. Microbiota composition was assessed in caecum content. Butyrate supplementation resulted in increased expression of tight junction proteins (ZO-1, claudin-7, E-cadherin), antimicrobial peptides (Defa 8, Rd5, RegIIIγ), and lysozyme in the ileal mucosa. Butyrate partially alleviated PN-induced intestinal barrier impairment and normalised IL-4, IL-10, and IgA mRNA expression. PN administration was associated with an increase in Tregs in MLN, which was normalised by butyrate. Butyrate increased the total number of CD4+ and decreased a relative amount of CD8+ memory T cells in MLN. Lack of enteral nutrition and PN administration led to a shift in caecal microbiota composition. Butyrate did not reverse the altered expression of most taxa but did influence the abundance of some potentially beneficial/pathogenic genera, which might contribute to its overall beneficial effect.

scholarly journals The effect of butyrate-supplemented parenteral nutrition on intestinal defence mechanisms and the parenteral nutrition-induced shift in the gut microbiota

2018 ◽  
Author(s):  
Z Jirsova ◽  
M Heczkova ◽  
H Dankova ◽  
H Malinska ◽  
P Videnska ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Parenteral Nutrition ◽  
Antimicrobial Peptides ◽  
Tight Junction ◽  
Microbiota Composition ◽  
Tight Junction Proteins ◽  
Defence Mechanisms ◽  
Altered Expression ◽  
Intestinal Immune System ◽  
Junction Proteins

AbstractButyrate produced by the intestinal microbiota is essential for proper functioning of the intestinal immune system. Total dependence on parenteral nutrition (PN) is associated with numerous adverse effects, including severe microbial dysbiosis and loss of important butyrate producers. We hypothesised that a lack of butyrate produced by the gut microbiota may be compensated by its supplementation in PN mixtures. We tested whetheri.v.butyrate administration would (a) positively modulate intestinal defence mechanisms and (b) counteract PN-induced dysbiosis. Male Wistar rats were randomised to chow, PN, and PN supplemented with 9 mM butyrate (PN+But) for 12 days. Antimicrobial peptides, mucins, tight junction proteins and cytokine expression were assessed by RT-qPCR. T-cell subpopulations in mesenteric lymph nodes (MLN) were analysed by flow cytometry. Microbiota composition was assessed in caecum content. Butyrate supplementation resulted in increased expression of tight junction proteins (ZO-1, claudin-7, E-cadherin), antimicrobial peptides (Defa 8, Rd5, RegIIIγ) and lysozyme in the ileal mucosa. Butyrate partially alleviated PN-induced intestinal barrier impairment and normalised IL-4, IL-10 and IgA mRNA expression. PN administration was associated with an increase in Tregs in MLN, which was normalised by butyrate. Butyrate increased the total number of CD4+ and decreased a relative amount of CD8+ memory T cells in MLN. Lack of enteral nutrition and PN administration led to a shift in caecal microbiota composition. Butyrate did not reverse the altered expression of most taxa but did influence the abundance of some potentially beneficial/ pathogenic genera, which might contribute to its overall beneficial effect.

Holly polyphenols alleviate intestinal inflammation and alter microbiota composition in lipopolysaccharide-challenged pigs

2020 ◽  
Vol 123 (8) ◽  
pp. 881-891 ◽  
Author(s):  
Xiao Xu ◽  
Hongwei Hua ◽  
Longmei Wang ◽  
Pengwei He ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Tight Junction ◽  
Intestinal Inflammation ◽  
Basal Diet ◽  
16S Rrna Gene Sequencing ◽  
Intestinal Injury ◽  
Rrna Gene ◽  
Microbiota Composition ◽  
Tight Junction Proteins ◽  
Lps Challenge ◽  
Junction Proteins

AbstractThe effect of holly polyphenols (HP) on intestinal inflammation and microbiota composition was evaluated in a piglet model of lipopolysaccharide (LPS)-induced intestinal injury. A total of twenty-four piglets were used in a 2 × 2 factorial design including diet type and LPS challenge. After 16 d of feeding with a basal diet supplemented with or without 250 mg/kg HP, pigs were challenged with LPS (100 μg/kg body weight) or an equal volume of saline for 4 h, followed by analysis of disaccharidase activities, gene expression levels of several representative tight junction proteins and inflammatory mediators, the SCFA concentrations and microbiota composition in intestinal contents as well as proinflammatory cytokine levels in plasma. Our results indicated that HP enhanced intestinal disaccharidase activities and reduced plasma proinflammatory cytokines including TNF-α and IL-6 in LPS-challenged piglets. Moreover, HP up-regulated mRNA expression of intestinal tight junction proteins such as claudin-1 and occludin. In addition, bacterial 16S rRNA gene sequencing showed that HP altered hindgut microbiota composition by enriching Prevotella and enhancing SCFA production following LPS challenge. These results collectively suggest that HP is capable of alleviating LPS-triggered intestinal injury by improving intestinal disaccharidase activities, barrier function and SCFA production, while reducing intestinal inflammation.

Direct effects of fermented cow’s milk product with Lactobacillus paracasei CBA L74 on human enterocytes

2018 ◽  
Vol 9 (1) ◽  
pp. 165-172 ◽  
Author(s):  
L. Paparo ◽  
R. Aitoro ◽  
R. Nocerino ◽  
C. Fierro ◽  
C. Bruno ◽  
...  
Keyword(s):  
Cell Growth ◽  
Infectious Diseases ◽  
Tight Junction ◽  
Layer Thickness ◽  
Immune Defence ◽  
Mucus Layer ◽  
Tight Junction Proteins ◽  
Defence Mechanisms ◽  
Mucin 2 ◽  
Junction Proteins

Cow’s milk fermented with Lactobacillus paracasei CBA L74 (FM-CBAL74) exerts a preventive effect against infectious diseases in children. We evaluated if this effect is at least in part related to a direct modulation of non-immune and immune defence mechanisms in human enterocytes. Human enterocytes (Caco-2) were stimulated for 48 h with FM-CBAL74 at different concentrations. Cell growth was assessed by colorimetric assay; cell differentiation (assessed by lactase expression), tight junction proteins (zonula occludens1 and occludin), mucin 2, and toll-like receptor (TRL) pathways were analysed by real-time PCR; innate immunity peptide synthesis, beta-defensin-2 (HBD-2) and cathelicidin (LL-37) were evaluated by ELISA. Mucus layer thickness was analysed by histochemistry. FMCBA L74 stimulated cell growth and differentiation, tight junction proteins and mucin 2 expression, and mucus layer thickness in a dose-dependent fashion. A significant stimulation of HBD-2 and LL-37 synthesis, associated with a modulation of TLR pathway, was also observed. FM-CBAL74 regulates non-immune and immune defence mechanisms through a direct interaction with the enterocytes. These effects could be involved in the preventive action against infectious diseases demonstrated by this fermented product in children.

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.

Altered expression of tight junction proteins in mammary epithelium after discontinued suckling in mice

2011 ◽  
Vol 463 (2) ◽  
pp. 391-398 ◽  
Author(s):  
Alexander G. Markov ◽  
Natalia M. Kruglova ◽  
Yulia A. Fomina ◽  
Michael Fromm ◽  
Salah Amasheh
Keyword(s):  
Tight Junction ◽  
Mammary Epithelium ◽  
Tight Junction Proteins ◽  
Altered Expression ◽  
Junction Proteins

scholarly journals Dietary protocatechuic acid ameliorates inflammation and up-regulates intestinal tight junction proteins by modulating gut microbiota in LPS-challenged piglets

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ruizhi Hu ◽  
Ziyu He ◽  
Ming Liu ◽  
Jijun Tan ◽  
Hongfu Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gut Microbiota ◽  
Tight Junction ◽  
Protocatechuic Acid ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Serum Levels ◽  
Intestinal Barrier Function ◽  
Tight Junction Proteins ◽  
Junction Proteins

Abstract Background Weaning is one of the major factors that cause stress and intestinal disease in piglets. Protocatechuic acid (PCA) is an active plant phenolic acid which exists in Chinese herb, Duzhong (Eucommia ulmoides Oliver), and is also considered as the main bioactive metabolite of polyphenol against oxidative stress and inflammation. This study aimed to investigate the effect of PCA on growth performance, intestinal barrier function, and gut microbiota in a weaned piglet model challenged with lipopolysaccharide (LPS). Methods Thirty-six piglets (Pig Improvement Company line 337 × C48, 28 d of age, 8.87 kg ± 0.11 kg BW) were randomly allocated into 3 treatments and fed with a basal diet (CTL), a diet added 50 mg/kg of aureomycin (AUR), or a diet supplemented with 4000 mg/kg of PCA, respectively. The piglets were challenged with LPS (10 μg/kg BW) on d 14 and d 21 by intraperitoneal injection during the 21-d experiment. Animals (n = 6 from each group) were sacrificed after being anesthetized by sodium pentobarbital at 2 h after the last injection of LPS. The serum was collected for antioxidant indices and inflammatory cytokines analysis, the ileum was harvested for detecting mRNA and protein levels of tight junction proteins by PCR and immunohistochemical staining, and the cecum chyme was collected for intestinal flora analysis using 16S rRNA gene sequencing. Results Dietary supplementation of PCA or AUR significantly increased the expression of tight junction proteins including ZO-1 and claudin-1 in intestinal mucosa, and decreased the serum levels of thiobarbituric acid reactive substances (TBARS) and IL-6, as compared with CTL group. In addition, PCA also decreased the serum levels of IL-2 and TNF-α (P < 0.05). Analysis of gut microbiota indicated that PCA increased the Firmicutes/Bacteroidetes ratio (P < 0.05). Spearman’s correlation analysis at the genus level revealed that PCA reduced the relative abundance of Prevotella 9, Prevotella 2, Holdemanella, and Ruminococcus torques group (P < 0.05), and increased the relative abundance of Roseburia and Desulfovibrio (P < 0.05), whereas AUR had no significant effect on these bacteria. Conclusions These results demonstrated that both PCA and AUR had protective effect on oxidative stress, inflammation and intestinal barrier function in piglets challenged with LPS, and PCA potentially exerted the protective function by modulating intestinal flora in a way different from AUR. Holdemanella

scholarly journals Capsaicin Improves The Hypoglycemic Effect of Metformin Benefitted From Gut Microbiota

2021 ◽  
Author(s):  
Zhi-Qiang Kang ◽  
Jing-Lei Hu ◽  
Man-Yun Chen ◽  
Yu Mao ◽  
Li-Fang Xie ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Tight Junction ◽  
Inflammatory Cytokines ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
Hypoglycemic Effect ◽  
Tight Junction Proteins ◽  
Inflammatory Infiltration ◽  
Blood Biochemical ◽  
Junction Proteins

Abstract Background: Capsaicin(CAP) possesses a hypoglycemic activity through remodulating gut microbiota as well as the first-line oral hypoglycemic drug, metformin(MET). However, CAP on the hypoglycemic effect of MET pertinent to gut microbiota remained poorly known.Methods: The glucose and insulin tolerance of diabetic rats were monitored. The glycolipid metabolism were analyzed by detecting blood biochemical parameters. Liver pathological changes were observed by HE staining. The inflammatory cytokines and intestinal tight junction proteins were detected by RT-PCR and Western blot. 16S rRNA sequencing was employed to analyze gut microbiota.Results: Compared with MET monotherapy, CAP and MET co-treatment could significantly reduce fasting blood glucose, improve glucose tolerance, lessen the degree of liver injury and inflammatory infiltration, reduce the expression of inflammatory cytokines and increase the expression of intestinal tight junction proteins in diabetic rats. Moreover, CAP and MET co-treatment altered gut microbiota profiles by regulating microbial abundances such as Akkermansia.Conclusion: CAP showed significant hypoglycemic effect of MET benefitted from remodulating gut microbiota in diabetic rats.

Altered Expression of Tight Junction Proteins in Cyclosporine Nephrotoxicity

2011 ◽  
Vol 33 (1) ◽  
pp. 7-16 ◽  
Author(s):  
Chang Hwa Lee ◽  
Sua Kim ◽  
Chong Myung Kang ◽  
Wan Young Kim ◽  
Jin Kim ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Proteins ◽  
Altered Expression ◽  
Cyclosporine Nephrotoxicity ◽  
Junction Proteins
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