Project description:This study investigated the impact of a high cellulose diet (HCD) on intestinal homeostasis and food allergy development in BALB/c mice. While soluble fibers are known to mitigate FA via short-chain fatty acid (SCFA) production, the role of insoluble fibers like cellulose remains unclear. Mice fed HCD exhibited gut dysbiosis, characterized by increased Proteobacteria, decreased tight junction protein expression, and intestinal barrier impairment, despite unchanged SCFA levels. RNA sequencing revealed HCD-induced upregulation of immune pathways, including the positive regulation of B and T cells differentiation and antigen receptor-mediated signaling pathway. Following ovalbumin (OVA) sensitization, HCD-fed mice displayed exacerbated allergic symptoms, including elevated OVA-specific IgE, IgG, histamine, and mMCP-1 levels. Gut microbiota analysis highlighted enrichment of potentially pathogenic taxa in HCD+OVA groups. Fecal microbiota transplantation (FMT) from HCD donors to antibiotic-treated recipients showed severe food allergy responses, confirming microbiota-mediated effects. These findings demonstrate that HCD exacerbates food allergy through gut microbial dysbiosis, intestinal barrier disruption, and intestinal immune disorder.
Project description:Investigation of the effect of chow diet integration with standard baker's yeast leavened carasau bread (SB) or with functional sourdough-leavened carasau bread (FB) on the gut microbiota of young rats.
Project description:This study was performed to investigate the effect of aging and high fat diet on gut microbiota in F344 rats by the pyrosequencing method.
Project description:Gut microbiota dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.
Project description:The postnatal period is one of the important windows for developing the gastrointestinal tract's structure-function and associated mucosal immunity. Recent studies suggest a promising contribution of gut microbiota in maintaining host health, immunity, and gut development. However, the function of postnatal gut microbiota dynamics concerning intestinal mucosal development needs to be better understood. To decipher the causal role of gut microbiota on barrier integrity and intestinal epithelium development, we executed an antibiotic-mediated perturbation and tracked the kinetics in postnatal mice. We observed a postnatal age-related impact of antibiotic-mediated gut microbiota perturbation with a substantial decrease in total bacterial load on P14D and also in the barrier integrity and IECs marker. To enhance our knowledge of the mechanisms behind this, we employed a global transcriptomics approach to see the alterations in the mucosal innate immunity and other relevant pathways.
Project description:Purpose: Gut microbiota is associated with the progression of brain tumor. However, the alterations in the gut microbiota during glioma growth and temozolomide (TMZ) therapy remains to be understood. Methods: C57BL/6 male mice were implanted with GL261 glioma cells. TMZ/sodium carboxymethyl cellulose (SCC) was administered by gavage for five consecutive days (from 8 to 12 days after implantation). Fecal samples were collected before (T0) and on days 7 (T1), 14 (T2), and 28 (T3) after implantation. The gut microbiota was analyzed using 16S ribosomal DNA sequencing followed by absolute and relative quantitation analyses. Results: Nineteen genera were altered during glioma progression with the most dramatic changes in Firmicutes and Bacteroidetes phyla. During glioma growth, Lactobacillus abundance decreased at the earlier stage of glioma development (T1), and then gradually increased (T2, T3); Intestinimonas abundance exhibited a persistent increase; Anaerotruncus showed a transient increase and then a subsequent decrease. Twenty genera altered following TMZ treatment. The enrichment of Akkermansia and Bifidobacterium was observed only at the early stage following TMZ treatment (T2), but not at the later stage (T3). Additionally, the decrease of Anaerotruncus was slighter in TMZ group at T3 comparing to the vehicle group. The abundance of Intestinimonas increased constantly during the progression of glioma, but was unaffected by TMZ. Conclusions: Glioma development and progression resulted in altered gut microbiota. TMZ reversed the decrease of Anaerotruncus in glioma at T3, and increased the abundance of Bifidobacterium with no influence on the increase of Intestinimonas. Short-term and long-term effects of TMZ treatment on the bacterial communities may be differential. This study will improve understanding the role of gut microbiota in glioma, and help develop gut microbiota as a potential therapeutic target.