Butyrate administration strengthens the intestinal epithelium and improves intestinal dysbiosis in a cholestasis fibrosis model

Abstract

Aim Intestinal dysfunction in cirrhosis patients is linked to death by bacterial infections. Currently, there is no effective therapy for this complication. This study aims to evaluate butyrate, a novel postbiotic, on the intestinal inflammatory response, tight junction proteins and the microbiota in the cholestasis model. Methods and Results Wistar rats underwent 15 days of bile duct ligation (BDL). We administered butyrate at a concentration of 1%. The BDL group did not receive treatment. The results showed that butyrate could significantly reduce pro‐inflammatory cytokines (IL‐17A, IFN‐γ, TNF‐α) in the ileum and colon while promoting IL‐10 expression in the colon. Moreover, it significantly promotes tight junction protein (cld‐1, occludin and ZO‐1) expression in the ileum. A similar effect was observed in the colon except for ZO‐1. Additionally, butyrate limited taxa diversity loss and promoted probiotic genera expansion such as Lachnospira, Prevotella and Lactobacillus. The increase in Turicibacter and Clostridiaceae distinguished the BDL group. Conclusions Butyrate is effective in regulating the inflammatory response, tight junction proteins and limits bacterial diversity loss. Significance and Impact of the Study This research reveals that butyrate could represent an interesting postbiotic metabolomic intervention for intestinal epithelium dysfunction in liver disease.

Escherichia/Shigella, SCFAs, and Metabolic Pathways—The Triad That Orchestrates Intestinal Dysbiosis in Patients with Decompensated Alcoholic Cirrhosis from Western Mexico

“…Considering this, our research group has recently demonstrated that the supplementation with butyrate exerts beneficial effects on the intestinal epithelium, positively regulating tight junction proteins, mitigating the immune response, and limiting the loss of bacterial diversity in the cholestasis experimental model [18].…”

“…Furthermore, SCFA are important contributors in processes implicated in the pathophysiology of cirrhosis, such as the maintenance of a gut barrier function, immune regulation, anti-inflammatory effects, and the regulation of microbiota itself [16][17][18].…”

Bacteroides fragilis derived metabolites, identified by molecular networking, decrease Salmonella virulence in mice model

“…(B) Among them, cholic acid (CA) and deoxycholic acid were identified. TNF-α) in the gut and in other organs (Huang et al, 2021;Peña-Rodríguez et al, 2022;Yue et al, 2022). Desaminotyrosine, produced by Clostridium orbiscidens, can protect against influenza virus infection by increasing the expression of IFN-I way (Steed et al, 2017;Wei et al, 2020).…”

“…SCFAs, particularly butyrate and propionate, reduced inflammatory bowel diseases (IBD) and decreased inflammation in patients ( Silva et al, 2018 ; Li et al, 2021 ). These compounds were shown to increase the expression of cell junction genes and to decrease that of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) in the gut and in other organs ( Huang et al, 2021 ; Peña-Rodríguez et al, 2022 ; Yue et al, 2022 ). Desaminotyrosine, produced by Clostridium orbiscidens , can protect against influenza virus infection by increasing the expression of IFN-I way ( Steed et al, 2017 ; Wei et al, 2020 ).…”

Role of Intestinal Dysbiosis and Nutrition in Rheumatoid Arthritis

“…Pena-Rodriguez et al studied the effect of butyrate on the intestinal inflammatory response in a cholestasis model. Administration of butyrate was found to reduce pro-inflammatory cytokines and upregulate the production of tight junction proteins [ 99 ]. Berberine, a therapeutic option in treating type-2 diabetes, increased SCFA-producing bacteria and lowered gut inflammation [ 100 ].…”