Project description:Recent evidence suggests an important role of the gut microbiome in early life on immune cell entraining. Using two independent transgenic (Tg) lines of Alzheimer’s disease, we have demonstrated that life-long antibiotic (ABX)-perturbation of the gut microbiome is associated with reduced amyloid beta (Ab) plaque pathology and microglial phenotypes in male mice. Furthermore, fecal microbiota transfer (FMT) from age-matched APPPS1-21 Tg mice into long-term ABX-treated male APPPS1-21 mice partially restored amyloidosis and microgliosis, thus establishing causality. in the current studies, we planned to investigate the transcriptome profiles in APPPS1-21 mice treated with short-term abx (PND14-21) compared with vehicle treated groups in genotype-, sex- and time -dependent manner. Most importantly, we also investigated if fecal microbiota transplants from age-matched Tg male mice into short-term abx (PND14-21)-treated male mice restores brain transcriptomes to that of obsreved in vehicle-treated male mice at 9 weeks of age.
Project description:Analysis of breast cancer survivors' gut microbiota after lifestyle intervention, during the COVID-19 lockdown, by 16S sequencing of fecal samples.
Project description:We found that low protein diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that low protein diet could negatively affect Paneth cell function. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.
Project description:D-galactose orally intake ameliorate DNCB-induced atopic dermatitis by modulating microbiota composition and quorum sensing. The increased abundance of bacteroidetes and decreased abundance of firmicutes was confirmed. By D-galactose treatment, Bacteroides population was increased and prevotella, ruminococcus was decreased which is related to atopic dermatitis.
Project description:Although modern clinical practices such as cesarean sections and perinatal antibiotics have improved infant survival, treatment with broad-spectrum antibiotics alters intestinal microbiota and causes dysbiosis. Infants exposed to perinatal antibiotics have an increased likelihood of life-threatening infections, including pneumonia. Here, we investigated how the gut microbiota sculpt pulmonary immune responses, promoting recovery and resolution of infection in newborn rhesus macaques. Early-life antibiotic exposure interrupted the maturation of intestinal commensal bacteria and disrupted the developmental trajectory of the pulmonary immune system, as assessed by single-cell proteomic and transcriptomic analyses. Early-life antibiotic exposure rendered newborn macaques more susceptible to bacterial pneumonia, concurrent with increases in neutrophil senescence and hyperinflammation, broad inflammatory cytokine signaling, and macrophage dysfunction. This pathogenic reprogramming of pulmonary immunity was further reflected by a hyperinflammatory signature in all pulmonary immune cell subsets coupled with a global loss of tissue-protective, homeostatic pathways in the lungs of dysbiotic newborns. Fecal microbiota transfer was associated with partial correction of the broad immune maladaptations and protection against severe pneumonia. These data demonstrate the importance of intestinal microbiota in programming pulmonary immunity and support the idea that gut microbiota promote the balance between pathways driving tissue repair and inflammatory responses associated with clinical recovery from infection in infants. Our results highlight a potential role for microbial transfer for immune support in these at-risk infants.