Dataset Information

Sodium Butyrate Modulates Mucosal Inflammation Injury Mediated by GPR41/43 in the Cecum of Goats Fed a High Concentration Diet.

ABSTRACT: Emerging data indicate that excessive short chain fatty acids can mediate the downstream mitogen-activated protein kinase pathways by activating G-protein coupled receptor 41/43 (GPR41/43) to initiate the inflammatory response. The current study was conducted to investigate if a high concentrate (HC) supplemented with sodium butyrate can alleviate the inflammation and if an epigenetic mechanism is involved in regulating the expression of the key GPR41/43 genes in the cecum. Twelve lactating goats were randomly divided into two groups: the control group fed the HC diet and the treatment group fed the HC diet supplemented with sodium butyrate (HCB). Our results suggested that the supplementation of sodium butyrate significantly increased the pH value in the rumen and cecum, downregulated the expression of GPR41/43 and related inflammatory cytokines, upregulated the expression of tight junction proteins, and reduced the protein expression levels of GPR 41/43, ERK1/2, and p38. Moreover, the ratios of DNA methylation and chromatin compaction in the promoter region of the GPR41/43 genes were altered due to the addition of sodium butyrate. In brief, dietary addition of sodium butyrate can reduce the inflammatory injury to the cecal mucosa in lactating goats and can affect the expression of GPR41/43 via epigenetic modification.

SUBMITTER: Chang G

PROVIDER: S-EPMC6729013 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Sodium Butyrate Modulates Mucosal Inflammation Injury Mediated by GPR41/43 in the Cecum of Goats Fed a High Concentration Diet.

Chang Guangjun G Ma Nana N Zhang Huanmin H Wang Yan Y Huang Jie J Liu Jing J Dai Hongyu H Shen Xiangzhen X

Frontiers in physiology 20190830

Emerging data indicate that excessive short chain fatty acids can mediate the downstream mitogen-activated protein kinase pathways by activating G-protein coupled receptor 41/43 (GPR41/43) to initiate the inflammatory response. The current study was conducted to investigate if a high concentrate (HC) supplemented with sodium butyrate can alleviate the inflammation and if an epigenetic mechanism is involved in regulating the expression of the key GPR41/43 genes in the cecum. Twelve lactating goat ...[more]

PMID: 31543829

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Project description:BackgroundChronic rhinosinusitis (CRS) is a heterogeneous chronic inflammatory disease generally divided based on the presence or absence of nasal polyps (NPs). One of the features of NPs is excessive fibrin deposition, which is associated with down-regulation of tissue plasminogen activator (t-PA) in NPs. As t-PA is expressed in epithelial cells, and epithelium is readily accessible to topical therapies, identifying compounds that can mediate the induction of t-PA would be a potential new strategy for the treatment of NPs.ObjectiveThe objective of this study was to determine whether short-chain fatty acids (SCFAs) can induce t-PA in airway epithelial cells via their known receptors GPR41 and GPR43.MethodsWe performed immunohistochemistry (IHC) to determine whether receptors for SCFAs, known as G protein-coupled receptor 41/free fatty acid receptor 3 (GPR41/FFAR3) and GPR43/FFAR2, are expressed in nasal tissue. Primary normal human bronchial epithelial (NHBE) cells were stimulated with different concentrations of SCFAs to test induction of t-PA, which was analysed by expression of mRNA and protein. Mediation of responses by SCFA receptors was evaluated by specific receptor gene silencing with siRNA.ResultsImmunohistochemistry study revealed that airway epithelial cells expressed GPR41 and GPR43. Acetic acid, propionic acid, butyric acid and valeric acid significantly induced t-PA expression from two- to tenfolds. The strongest inducer of t-PA from NHBE cells was propionic acid; cells stimulated with propionic acid released t-PA into the supernatant in its active form. Gene silencing of GPR41 and GPR43 revealed that induction of t-PA by SCFAs was dependent upon both GPR41 and GPR43.Conclusions and clinical relevanceShort-chain fatty acids were shown to induce airway epithelial cell expression of t-PA via GPR41 and GPR43. Topical delivery of potent compounds that activate these receptors may have value by reducing fibrin deposition and shrinking nasal polyp growth.

Project description:Our previous study indicated that dietary xylooligosaccharide (XOS) supplementation improved feed efficiency, ileal morphology, and nutrient digestibility in laying hens. The objective of this study was to evaluate the mitigative effects of XOS on intestinal mucosal barrier impairment and microbiota dysbiosis induced by oxidized fish oil (OFO) in laying hens. A total of 384 Hy-Line Brown layers at 50 weeks of age were randomly divided into four dietary treatments, including the diets supplemented with 20 g/kg of fresh fish oil (FFO group) or 20 g/kg of oxidized fish oil (OFO group), and the OFO diets with XOS addition at 200 mg/kg (OFO/XOS200 group) or 400 mg/kg (OFO/XOS400 group). Each treatment had eight replicates with 12 birds each. The OFO treatment decreased (P < 0.05) the production performance of birds from 7 to 12 weeks of the experiment, reduced (P < 0.05) ileal mucosal secretory immunoglobulin A (sIgA) content, and increased (P < 0.05) serum endotoxin concentration, as well as downregulated (P < 0.05) mRNA expression of claudin-1 (CLDN1) and claudin-5 (CLDN5) in the ileal mucosa at the end of the experiment. Dietary XOS addition (400 mg/kg) recovered (P < 0.05) these changes and further improved (P < 0.05) ileal villus height (VH) and the villus height-to-crypt depth ratio (VCR). In addition, OFO treatment altered cecal microbial composition of layers, and these alterations were probably involved in OFO-induced ileal mucosal impairment as causes or consequences. Supplemental XOS remodeled cecal microbiota of layers fed the OFO diet, characterized by an elevation in microbial richness and changes in microbial composition, including increases in Firmicutes, Ruminococcaceae, Verrucomicrobia (Akkermansia), Paraprevotella, Prevotella_9, and Oscillospira, along with a decrease in Erysipelatoclostridium. The increased abundance of Verrucomicrobia (Akkermansia) had positive correlations with the improved ileal VH and ileal mucosal expression of CLDN1. The abundance of Erysipelatoclostridium decreased by XOS addition was negatively associated with ileal VH, VCR, ileal mucosal sIgA content, and the relative expression of zonula occludens-2, CLDN1, and CLDN5. Collectively, supplemental XOS alleviated OFO-induced intestinal mucosal barrier dysfunction and performance impairment in laying hens, which could be at least partially attributed to the modulation of gut microbiota.

Dataset Information

Sodium Butyrate Modulates Mucosal Inflammation Injury Mediated by GPR41/43 in the Cecum of Goats Fed a High Concentration Diet.

Publications

Sodium Butyrate Modulates Mucosal Inflammation Injury Mediated by GPR41/43 in the Cecum of Goats Fed a High Concentration Diet.

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