Causality of gut bacteria Klebsiella pneumoniae to hypertension development II
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE209720 | GEO | 2023/07/31
REPOSITORIES: GEO
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Project description:Purpose: we conducted this study to investigate whether gut K.pn is a causal factor for HTN pathogenesis and the potential mechanism Methods: Renal transcriptome changes were assessed by RNA-sequencing Results: significant upregulation of several genes related to HTN pathogenesis were observed Conclusions:These results provide evidence that the enrichment of K.pn acts as a direct contributor for hypertension pathogenesis
2022-09-30 | GSE184584 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE25572: Depolymerization of plant cell wall glycans by symbiotic human gut bacteria (Bacteroides thetaiotaomicron) GSE25575: Depolymerization of plant cell wall glycans by symbiotic human gut bacteria (Bacteroides ovatus) Refer to individual Series
2011-05-01 | E-GEOD-25576 | biostudies-arrayexpress
Project description:The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
2024-01-31 | GSE248692 | GEO
Project description:The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
2024-01-31 | GSE248691 | GEO
Project description:The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
2024-01-31 | GSE248690 | GEO
Project description:To evaluate the specific changes that renal LECs undergo in hypertension (HTN), we performed single-cell RNA sequencing. Using the angiotensin II-induced and salt-sensitive mouse models of HTN, we isolated renal CD31+ and podoplanin+ cells from hypertensive and normotensive mice. Sequencing of these cells revealed three distinct cell types (LECs, myeloid immune cells, and an unusual third population we dubbed multipotent nephron-associated support cells) with unique expression profiles.
2024-05-14 | GSE236410 | GEO
Project description:Approximately 15% of US adults have circulating levels of uric acid above its solubility limit, which is causally linked to the inflammatory disease gout. In most mammals, uric acid elimination is facilitated by the enzyme uricase. However, human uricase is a pseudogene, having been inactivated early in hominid evolution. Though it has long been known that a substantial amount of uric acid is eliminated in the gut, the role of the gut microbiota in hyperuricemia has not been studied. Here we identify a gene cluster, widely distributed in the gut microbiome, that encodes a pathway for uric acid degradation. Stable isotope tracing demonstrates that gut bacteria metabolize uric acid to xanthine or short chain fatty acids such as acetate, lactate and butyrate. Ablation of the microbiota in uricase-deficient mice causes profound hyperuricemia, and anaerobe-targeted antibiotics increase the risk of gout in humans. These data reveal a role for the gut microbiota in uric acid excretion and highlight the potential for microbiome-targeted therapeutics in hyperuricemia.
2023-06-16 | GSE206419 | GEO
Project description:The gut microbiome is a malleable microbial community that can remodel in response to various factors, including diet, and contribute to the development of several chronic diseases, including atherosclerosis. We devised an in vitro screening protocol of the mouse gut microbiome to discover molecules that can selectively modify bacterial growth. This approach was used to identify cyclic D,L-α-peptides that remodeled the Western diet (WD) gut microbiome toward the low-fat-diet microbiome state. Daily oral administration of the peptides in WD-fed LDLr-/- mice reduced plasma total cholesterol levels and atherosclerotic plaques. Depletion of the microbiome with antibiotics abrogated these effects. Peptide treatment reprogrammed the microbiome transcriptome, suppressed the production of pro-inflammatory cytokines (including interleukin-6, tumor necrosis factor-α and interleukin-1β), rebalanced levels of short-chain fatty acids and bile acids, improved gut barrier integrity and increased intestinal T regulatory cells. Directed chemical manipulation provides an additional tool for deciphering the chemical biology of the gut microbiome and might advance microbiome-targeted therapeutics.
2019-12-31 | GSE104913 | GEO
Project description:Non-enzymatic activation of renin via its interaction with prorenin receptor (PRR) has been proposed as a key mechanism of local renin-angiotensin system (RAS) activation. The presence of renin and angiotensinogen has been reported in the rostral ventrolateral nucleus (RVLM). Overactivation of bulbospinal neurons RVLM is linked to hypertension (HTN). Previous studies have shown that the brain RAS plays a role in the pathogenesis of the deoxycorticosterone (DOCA)-salt HTN model. Thus, we hypothesized that PRR in the RVLM is involved in the local activation of the RAS, facilitating the development of DOCA-salt HTN. Selective PRR ablation targeting the RVLM (PRRRVLM-Null mice) resulted in an unexpected sex-dependent and biphasic phenotype in DOCA-salt HTN. That is, PRRRVLM-Null females (but not males) exhibited a significant delay in achieving maximal pressor responses during the initial stage of DOCA-salt HTN. Female PRRRVLM-Null subsequently showed exacerbated DOCA-salt-induced pressor responses during the “maintenance” phase with a maximal peak at 13 days on DOCA-salt. This exacerbated response was associated with an increased sympathetic drive to the resistance arterioles and the kidney, exacerbated fluid and sodium intake and output in response to DOCA-salt, and induced mobilization of fluids from the intracellular to extracellular space concomitant with elevated vasopressin. Ablation of PRR suppressed genes involved in RAS activation and catecholamine synthesis in the RVLM but also induced expression of genes involved in inflammatory responses. This study illustrates complex and sex-dependent roles of PRR in the neural control of BP and hydromineral balance through autonomic and neuroendocrine systems.
2023-09-14 | GSE235234 | GEO
Project description: Not available
| S-EPMC7604597 | biostudies-literature