Project description:The effect of oral microbiota on the intestinal microbiota has garnered growing attention as a mechanism linking periodontal diseases to systemic diseases. However, the salivary microbiota is diverse and comprises numerous bacteria with a largely similar composition in healthy individuals and periodontitis patients. Thus, the systemic effects of small differences in the oral microbiota are unclear. In this study, we explored how health-associated and periodontitis-associated salivary microbiota differently colonized the intestine and their subsequent systemic effects by analyzing the hepatic gene expression and serum metabolomic profiles. The salivary microbiota was collected from a healthy individual and a periodontitis patient and gavaged into C57BL/6NJcl[GF] mice. Samples were collected five weeks after administration. Gut microbial communities were analyzed by 16S ribosomal RNA gene sequencing. Hepatic gene expression profiles were analyzed using a DNA microarray and quantitative polymerase chain reaction. Serum metabolites were analyzed by capillary electrophoresis time-of-flight mass spectrometry. The gut microbial composition at the genus level was significantly different between periodontitis-associated microbiota-administered (PAO) and health-associated oral microbiota-administered (HAO) mice. The hepatic gene expression profile demonstrated a distinct pattern between the two groups, with higher expression of Neat1, Mt1, Mt2, and Spindlin1, which are involved in lipid and glucose metabolism. Disease-associated metabolites such as 2-hydroxyisobutyric acid and hydroxybenzoic acid were elevated in PAO mice. These metabolites were significantly correlated with Bifidobacterium, Atomobium, Campylobacter, and Haemophilus, which are characteristic taxa in PAO mice. Conversely, health-associated oral microbiota were associated with higher levels of beneficial serum metabolites in HAO mice. The multi-omics approach used in this study revealed that periodontitis-associated oral microbiota is associated with the induction of disease phenotype when they colonized the gut of germ-free mice.
Project description:Gut microbiota are known to influence oral drug disposition, yet the specific host pathways they affect remain poorly characterized. This study provides a transcriptome-wide characterization of how physiological gut microbiota regulate the expression of intestinal transporters, phase I and phase II metabolic enzymes, and barrier machinery relevant to oral drug disposition. By identifying microbiota-responsive processes, this work defines the scope of inter-individual variability attributable to gut microbial effects.
Project description:Those FASTQ are used in a paper where are primarily compared the variations in the oral microbiota composition between HIV patients and healthy controls (HC). In addition, it is performed a longitudinal evaluation of the oral-gut microbiota-immunity axis from HIV-infected patients before starting ART (T0) and after reaching virological suppression (T24 weeks).
Project description:The postnatal microbiota-immune axis establishes lifelong homeostasis at mucosal epithelial barriers. However, whether barrier-specific physiological activities regulate this process remains ill-defined. During weaning, the oral epithelium, which is monitored by Langerhans cells (LCs), is challenged by the development of a microbial plaque and the initiation of masticatory forces capable of damaging the epithelium. We demonstrate that microbial colonization following birth facilitates the differentiation of oral LCs, setting the stage for the weaning period, where adaptive immunity develops. Despite the presence of the challenging microbial plaque, LCs mainly respond to masticatory mechanical forces, inducing adaptive immunity to maintain epithelial integrity that is also associated with bone loss. Unlike adult life, this bone loss is IL-17-independent, suggesting that the establishment and maintenance of oral mucosal homeostasis involve distinct mechanisms. Moreover, barrier-specific features play a fundamental role in this early-life process.