Project description:Accumulating evidence suggests a strong link between intestinal microbiota and colorectal cancer initiation, beyond genetic factors. The origins of dysbiosis (altered microbiota composition) remain poorly understood, especially in genetically susceptible hosts. Our previous study has demonstrated that the presence of intraepithelial bacteria as a consequence of intestinal barrier dysfunction shaped dysbiotic microbiota that contributed to colitis development. Here, we evaluated the fecal and epithelial microbiota in age-matched Apc(Min/+) and wild-type littermates. The fecal samples and purified epithelial cells from intestinal segments (ileum and colon) were collected at various time points for analysis of microbiota composition by PacBio full-length 16S rRNA gene sequencing.
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:This study aimed to analyze changes in gut microbiota composition in mice after transplantation of fecal microbiota (FMT, N = 6) from the feces of NSCLC patients by analyzing fecal content using 16S rRNA sequencing, 10 days after transplantation. Specific-pathogen-free (SPF) mice were used for each experiments (N=4) as controls.
Project description:Cognitive impairment is a hallmark phenotype of methamphetamine (Meth) abuse, yet the cellular mechanisms driving these deficits remain poorly understood. This study aims to investigate the cellular composition, gene expression profiles, key signaling pathways, intercellular communication networks, and transcription factor activity in hippocampal tissues from control mice and those acutely exposed to Meth, thereby elucidating the mechanistic underpinnings of Meth-induced neurotoxicity. Single-nucleus RNA sequencing (snRNA-seq) was employed to investigate the transcriptomes of nuclei isolated from the hippocampus of acute Meth-treated and control mice. Our study provides a systemic understanding of the transcriptome alterations induced by Meth exposure in mouse hippocampus, which may offer clues for therapeutic strategies against acute Meth exposure.
Project description:We found that western diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet could negatively affect Paneth cell function. Subsequent generations of western diet consumption further reduced percentages of normal Paneth cell population. 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:In this study we investigated whether gut microbiota profile of Italian healthy volunteers could differ based on their geaographical origin. To this purpose, fecal samples were collected from 31 healthy individuals living in 3 different italian regions (Lombardy, North; Lazio, Center; Apulia, South) and their respective microbiota profiles were analyzed employing 16S metagenomic sequencing method. This study identifies differences in the gut microbiota content and richness among individuals with the same ethnicity coming from three different Italian regions.
Project description:This project focuses on the neurotoxic effects of methamphetamine (METH) abuse and its impact on the central nervous system. Methamphetamine is a highly addictive synthetic drug that can cause severe cognitive and behavioral changes, as well as neurodegenerative diseases. We conducted transcriptome sequencing on METH-treated primary neurons from tree shrews to investigate the underlying mechanisms of METH-induced neuronal damage.
Project description:Methamphetamine (Meth) is a powerful illicit psychostimulant, widely used for recreational purposes. Besides disrupting the monoaminergic system and promoting oxidative brain damage, Meth also causes neuroinflammation, contributing to synaptic dysfunction and behavioral deficits. Aberrant activation of microglia, the largest myeloid cell population in the brain, is a common feature in neurological disorders triggered by neuroinflammation. In this study, we investigated the mechanisms underlying the aberrant activation of microglia elicited by Meth in the adult mouse brain. We found that binge Meth exposure caused microgliosis and disrupted risk assessment behavior (a feature that usually occurs in individuals who abuse Meth), both of which required astrocyte-to-microglia crosstalk. Mechanistically, Meth triggered a detrimental increase of glutamate exocytosis from astrocytes (in a process dependent on TNF production and calcium mobilization), promoting microglial expansion and reactivity. Ablating TNF production, or suppressing astrocytic calcium mobilization, prevented microglia reactivity and abolished the behavioral phenotype elicited by Meth in the elevated plus maze (EPM). Overall, our data indicate that glial crosstalk is critical to relay alterations caused by acute Meth exposure.
