Undefined
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB57688 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR10497300.fastq.gz | Fastqsanger.gz | |||
| ERR10497400.fastq.gz | Fastqsanger.gz | |||
| ERR10497301.fastq.gz | Fastqsanger.gz | |||
| ERR10497401.fastq.gz | Fastqsanger.gz | |||
| ERR10497302.fastq.gz | Fastqsanger.gz |
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Project description:Mice with an intestinal epithelial specific knockout of LSD1 have changes in the intestinal epithelium including loss of Paneth and Goblet cells along with a general status of epithelial immaturity. To assess the influence of these epithelial specific changes on the mucosal immune system we performed a scRNAseq on CD45+ immune cells from the small intestine of mice with an epithelial specific LSD1 deletion (Villin-Cre+; Lsd1f/f) and wild type mice (Villin-Cre -; Lsd1f/f). To rule out a possible influence of the bacterial microbiome in the observed changes in CD45+ cell types we performed the same experiment in mice treated with antibiotics. These data allowed us to pinpoint changes in the cell populations of the mucosal immune system upon loss of LSD1 in the intestinal epithelium such as IgA producing cells and ILCs.
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Project description:The diverse bacterial communities that colonize the gastrointestinal tract play an essential role in maintaining immune homeostasis through the production of critical metabolites such as short chain fatty acids (SCFA), and this can be disrupted by antibiotic use. However, few studies have addressed the effects of specific antibiotics longitudinally on the microbiome and immunity. We evaluated the effects of four specific antibiotics; enrofloxacin, cephalexin, paromomycin, and clindamycin; in healthy female rhesus macaques. All antibiotics disrupted the microbiome, including reduced abundances of fermentative bacteria and increased abundances of potentially pathogenic bacteria, including Enterobacteriaceae in stool, and decreased Helicobacteraceae in the colon. This was associated with decreased SCFAs, indicating altered bacterial metabolism. Importantly, antibiotic use also substantially altered local immune responses, including increased neutrophils and Th17 cells in the colon. Furthermore, we observed increased soluble-CD14 in plasma, indicating microbial translocation. These data provide a longitudinal evaluation of antibiotic-induced changes to the composition and function of colonic bacterial communities, associated with specific alterations in mucosal and systemic immunity.
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Project description:Recent studies in both mice and human have suggested that the gut microbiota could modulate tumor response to chemotherapeutic agents or immunotherapies. However, the underlying mechanism has not been well characterized. Here, we found that disruption of the intestinal microbiota with antibiotics impaired the anti-cancer efficacy of oxaliplatin, which was correlated with the reduction of lots of the intestinal microbial metabolites including butyrate, one of the short chain fatty acids. Re-supplementation of either the whole intestinal microbial metabolites or butyrate could rescue the therapeutic responses of oxaliplatin in the microbiota-destroyed tumor-bearing mice by modulating CD8+ T cell function in the tumor microenvironment. Further experiments showed butyrate boosted the anti-tumor cytotoxic CD8+ T cell responses through ID2, a key transcription regulator highly expressed by tumor-infiltrating CD8+ T cells. Butyrate induced ID2 expression in CD8+ T cells, while ID2 further promoted the proliferation and function of CD8+ T cells through IL-12 signaling. Together, our findings suggest that gut microbial metabolite butyrate could promote the anti-tumor therapeutic efficacy through the ID2-dependent regulation of CD8+ T cell immunity.
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