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Cereus sinensis Polysaccharide Alleviates Antibiotic-Associated Diarrhea Based on Modulating the Gut Microbiota in C57BL/6 Mice.

ABSTRACT: The present study investigated whether the purified polysaccharide from Cereus sinensis (CSP-1) had beneficial effects on mice with antibiotic-associated diarrhea (AAD). The effects of CSP-1 on gut microbiota were evaluated by 16S rRNA high-throughput sequencing. Results showed that CSP-1 increased the diversity and richness of gut microbiota. CSP-1 enriched Phasecolarctobacterium, Bifidobacterium and reduced the abundance of Parabacteroides, Sutterella, Coprobacillus to near normal levels, modifying the gut microbial community. Microbial metabolites were further analyzed by gas chromatography-mass spectrometry (GC-MS). Results indicated CSP-1 promoted the production of various short-chain fatty acids (SCFAs) and significantly improved intestinal microflora dysfunction in AAD mice. In addition, enzyme linked immunosorbent assay and hematoxylin-eosin staining were used to assess the effects of CSP-1 on cytokine levels and intestinal tissue in AAD mice. Results demonstrated that CSP-1 inhibited the secretion of interleukin-2 (IL-2), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and improved the intestinal barrier. Correspondingly, the daily records also showed that CSP-1 promoted recovery of diarrhea status score, water intake and body weight in mice with AAD. In short, CSP-1 helped alleviate AAD by regulating the inflammatory cytokines, altering the composition and richness of intestinal flora, promoting the production of SCFAs, improving the intestinal barrier as well as reversing the dysregulated microbiota function.

SUBMITTER: Cui M

PROVIDER: S-EPMC8711652 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The present study is undertaken to assess the alleviating effects of antimicrobial peptide cecropin A on inflammatory bowel disease (IBD) in C57BL/6 mice and changes in the gut microbiota, compared to an antibiotic gentamicin. Different doses of cecropin A were intraperitoneally injected into C57BL/6 mice for 5 days to determine the safe doses. The injection doses at ≤ 15 mg/kg showed no negative impact on the liver, heart, spleen, and kidney. The severe and moderate IBD mice model was successfully established via supplementation of 4 or 2.5% dextran sulfate sodium (DSS) in drinking water for 5 days. The severe IBD model was used to ensure the optimal therapeutic dose of cecropin A. Survival rate, body weight and disease activity index (DAI) scores were measured. Administration of 15 mg/kg, not 5 mg/kg cecropin A, for 5 days increased survival rate and decreased body weight loss of mice. The moderate IBD model was applied to investigate the mechanisms for cecropin A to alleviate inflammation in comparison to gentamicin. The mice were treated with 15 mg/kg cecropin A or 5 mg/kg gentamicin for 3 days. The levels of cytokines and related proteins in the colon were detected by ELISA and Western blotting. The microbiota in cecum contents were analyzed using 16S rRNA gene sequencing. The results showed that cecropin A and gentamicin relieved body weight loss, DAI, and gut mucosa disruption, while decreasing tumor necrosis factor-α (TNF-α), interlukin-1β (IL-1β), and interlukin-6 (IL-6) induced by DSS. In addition, cecropin A and gentamicin showed different effects on the gut microbiota structure. Both cecropin A and gentamicin decreased DSS-induced enrichment of Bacteroidaceae and Enterobacteriaceae. However, cecropin A showed a selective enrichment of Lactobacillus in contrast to gentamicin, which demonstrated a selective effect on Desulfovibrionaceae and Ruminococcaceae. Cecropin A alleviates IBD through decreasing harmful gut microflora and specifically enhancing beneficial gut microflora. The mechanism of this effect is different from gentamicin.

Project description:Tributyrin (TB) is a butyric acid precursor and has a key role in anti-inflammatory and intestinal barrier repair effects by slowly releasing butyric acid. However, its roles in gut microbiota disorder caused by antibiotics remain unclear. Herein, we established an intestinal microbiota disorder model using ceftriaxone sodium via gavage to investigate the effects of different TB doses for restoring gut microbiota and intestinal injury. First, we divided C57BL/6 male mice into two groups: control (NC, n = 8) and experimental (ABx, n = 24) groups, receiving gavage with 0.2 mL normal saline and 400 mg/mL ceftriaxone sodium solution for 7 d (twice a day and the intermediate interval was 6 h), respectively. Then, mice in the ABx group were randomly split into three groups: model (M, 0.2 mL normal saline), low TB group (TL, 0.3 g/kg BW), and high TB group (TH, 3 g/kg BW) for 11 d. We found that TB supplementation alleviated antibiotics-induced weight loss, diarrhea, and intestinal tissue damage. The 16S rRNA sequence analysis showed that TB intervention increased the α diversity of intestinal flora, increased potential short-chain fatty acids (SCFAs)-producing bacteria (such as Muribaculaceae and Bifidobacterium), and inhibited the relative abundance of potentially pathogenic bacteria (such as Bacteroidetes and Enterococcus) compared to the M group. TB supplementation reversed the reduction in SCFAs production in antibiotic-treated mice. Additionally, TB downregulated the levels of serum LPS and zonulin, TNF-α, IL-6, IL-1β and NLRP3 inflammasome-related factors in intestinal tissue and upregulated tight junction proteins (such as ZO-1 and Occludin) and MUC2. Overall, the adjustment ability of low-dose TB to the above indexes was stronger than high-dose TB. In conclusion, TB can restore the dysbiosis of gut microbiota, increase SCFAs, suppress inflammation, and ameliorate antibiotic-induced intestinal damage, indicating that TB might be a potential gut microbiota modulator.

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Cereus sinensis Polysaccharide Alleviates Antibiotic-Associated Diarrhea Based on Modulating the Gut Microbiota in C57BL/6 Mice.

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