Abundance Of Desulfovibrionaceae Research Articles

β-Sitosterol protects against food allergic response in BALB/c mice by regulating the intestinal barrier function and reconstructing the gut microbiota structure.

This study investigated whether β-sitosterol has anti-allergic activity and explored its potential mechanism, using ovalbumin (OVA) allergic mouse model. Results indicated that supplementation with β-sitosterol at 5-20 mg kg-1 day-1 for 7 weeks alleviated allergic symptoms and intestinal inflammation, and reduced serum OVA-specific immunoglobulin (Ig) E, IgG and histamine levels in sensitized mice. β-Sitosterol enhanced physical and biochemical barrier in the intestinal epithelium by upregulating tight junction proteins (claudin-1, occludin, and ZO-1) expression and promoting the secretion of regenerating islet-derived protein IIIγ and secretory IgA in mucous layer. Furthermore, β-sitosterol administration increased the levels of interleukin 10 and transforming growth factor-β secreted by regulatory T cells, while reducing T helper 2 cell associated factor levels in intestinal lamina propria. Additionally, the alpha and beta diversity analysis revealed that the structure and diversity of the intestinal flora in the β-sitosterol group tended to be normalized compared with the model group, and the number of biomarkers was reduced from 32 to 7. Moreover, the altered composition of gut microbiota in allergic mice was also reversed by β-sitosterol supplementation, characterized by an increase in abundance of Lactobacillaceae and Bifidobacteriaceae and a decrease in abundance of Desulfovibrionaceae. Consequently, β-sitosterol may prevent FA by ameliorating intestinal barrier function and remodeling the gut microbiota.

Butyric Acid Ameliorates Myocardial Fibrosis by Regulating M1/M2 Polarization of Macrophages and Promoting Recovery of Mitochondrial Function

BackgroundWe aimed to investigate the effect and mechanism of butyric acid on rat myocardial fibrosis (MF).Methods16S rRNA sequencing was used to analyze the gut microbiota characteristics of the Sham group and MF group. HPLC was applied to measure butyric acid in the feces and serum. In vitro, rat macrophages RMa-bm were stimulated with LPS and IL-4, respectively, and then butyrate was added to study the influences of butyrate on M1/M2 polarization and mitochondrial function of rat macrophages. The rat macrophages and rat myocardial fibroblasts were co-cultured to explore the effect of butyrate on rat myocardial fibroblasts. In addition, MF rats were fed with butyric acid diet.ResultsCompared with the Sham group, collagen deposition in the MF group was increased, and fibrosis was serious. The abundance of Desulfovibrionaceae and Helicobacteraceae in the MF group was increased compared with the Sham group. Gut epithelial cells were destroyed in the MF group compared with the Sham group. Compared with the Sham group, LPS content in the MF group was increased and butyric acid was decreased. Butyrate inhibited M1 and promoted M2. Furthermore, butyrate may promote mitochondrial function recovery by regulating M1/M2 polarization of macrophages. After adding butyrate, cell proliferation ability was decreased, and aging and apoptosis were increased, which indicated that butyrate inhibited rat myocardial fibroblasts activity. Moreover, butyric acid could protect mitochondria and improve the symptoms of rats with MF.ConclusionsButyric acid ameliorated MF by regulating M1/M2 polarization of macrophages and promoting recovery of mitochondrial function.

Typical gut indigenous bacteria in ICR mice fed a soy protein-based normal or low-protein diet

For patients with inflammatory bowel disease, cow’s milk allergy, and lactose intolerance, soymilk is a potential alternative to cow’s milk. In this study, we aimed to identify the effects of a soy protein-based low-protein diet on the body and organ weights and the gut microbiome of six-week-old mice fed a diet containing 20% (SP) or 5% (LP) soy protein for 14 days via 16S rRNA (V4) amplicon sequencing. Body weight gain (growth) and liver, spleen, and fat tissue weight were significantly suppressed by the LP diet. Operational taxonomic unit numbers and α-diversity were lower in the LP group than in the SP group. A principal coordinate analysis revealed differences in the gut microbiome compositions of SP and LP mice. The abundances of caecal Roseburia sp., Alistipes sp., and bacteria from the family Muribaculaceae were lower in the LP group than in the SP group. In contrast, the abundance of Desulfovibrionaceae, which is positively correlated with inflammation, was higher in the LP group than in the SP group. These results differed from the effects of a milk casein-based low-protein diet (reported previously). Based on these findings, we conclude that the undesirable effects of a low-protein diet and/or protein deficiency are related to changes in the gut microbiome composition and may differ depending on the kind of proteins used.

Both Gut Microbiota and Differentially Expressed Proteins Are Relevant to the Development of Obesity

Although the role of the gut microbiota in obesity has recently received considerable attention, the exact mechanism is unclear. This study was aimed at investigating the profiles of bacterial communities in fecal samples and differentially expressed proteins (DEPs) in the peripheral blood in mice fed a high-fat diet (HFD) and standard diet (SD) and at providing new insights into the pathogenesis of obesity. The profiles of bacterial communities in fecal samples and DEPs in the peripheral blood were characterized in mice fed HFD and SD, respectively. The levels of 3 DEPs increased in HFD mice. The alpha diversity was significantly lower after 4 and 12 weeks in HFD mice. The beta diversity was higher after 4, 8, and 12 weeks in HFD mice. A total of 16 gut bacterial clades were significantly different with the linear discriminant analysis (LDA) score higher than 4 over time. The relative abundance levels of Proteobacteria and Deferribacteres were higher, while those of Bacteroidetes and Firmicutes were lower in HFD mice at the phylum level. The relative abundance of Desulfovibrionaceae and Rikenellaceae increased in HFD mice at the family level. The relative abundance of the Bacteroidetes_S24-7_group and Lachnospiraceae was lower in HFD mice. The gut microbiota had a significant correlation with serum lipid indexes and expression of DEPs at the phylum and family levels. The changes in the gut microbiota of HFD mice and their associations with the levels of inflammatory proteins could be one of the major etiological mechanisms underlying obesity.