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Host-microbiome response to hyperbaric oxygen treatment in ulcerative colitis

ABSTRACT: Host-microbiome response to hyperbaric oxygen treatment in ulcerative colitis

PROVIDER: PRJNA638658 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11991281.fastq.gz	Fastqsanger.gz
	SRR11991282.fastq.gz	Fastqsanger.gz
	SRR11991283.fastq.gz	Fastqsanger.gz
	SRR11991284.fastq.gz	Fastqsanger.gz
	SRR11991285.fastq.gz	Fastqsanger.gz

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Host-microbiome response to hyperbaric oxygen treatment in ulcerative colitis

Project description:Pre- and post-hyperbaric oxygen sequencing of mucosal biopsies of ulcerative colitis patients to understand host response to hyperoxia

2025-02-19 | GSE152229 | GEO

The Host-Microbiome Response to Hyperbaric Oxygen Therapy in Ulcerative Colitis Patients.

Project description:Background & aimsHyperbaric oxygen therapy (HBOT) is a promising treatment for moderate-to-severe ulcerative colitis. However, our current understanding of the host and microbial response to HBOT remains unclear. This study examined the molecular mechanisms underpinning HBOT using a multi-omic strategy.MethodsPre- and post-intervention mucosal biopsies, tissue, and fecal samples were collected from HBOT phase 2 clinical trials. Biopsies and fecal samples were subjected to shotgun metaproteomics, metabolomics, 16s rRNA sequencing, and metagenomics. Tissue was subjected to bulk RNA sequencing and digital spatial profiling (DSP) for single-cell RNA and protein analysis, and immunohistochemistry was performed. Fecal samples were also used for colonization experiments in IL10-/- germ-free UC mouse models.ResultsProteomics identified negative associations between HBOT response and neutrophil azurophilic granule abundance. DSP identified an HBOT-specific reduction of neutrophil STAT3, which was confirmed by immunohistochemistry. HBOT decreased microbial diversity with a proportional increase in Firmicutes and a secondary bile acid lithocholic acid. A major source of the reduction in diversity was the loss of mucus-adherent taxa, resulting in increased MUC2 levels post-HBOT. Targeted database searching revealed strain-level associations between Akkermansia muciniphila and HBOT response status. Colonization of IL10-/- with stool obtained from HBOT responders resulted in lower colitis activity compared with non-responders, with no differences in STAT3 expression, suggesting complementary but independent host and microbial responses.ConclusionsHBOT reduces host neutrophil STAT3 and azurophilic granule activity in UC patients and changes in microbial composition and metabolism in ways that improve colitis activity. Intestinal microbiota, especially strain level variations in A muciniphila, may contribute to HBOT non-response.

| S-EPMC9117812 | biostudies-literature

Ulcerative colitis gene expressions file

Project description:Ulcerative colitis related gene expressions analysis in colonic biopsy samples from control and ulcerative colitis patients

2019-07-10 | GSE134025 | GEO

Methylation profiling in Ulcerative colitis

Project description:The series was designed to identify the different methylated single CpGs involved in the pathophysiology of ulcerative colitis. A cohort of n=20 monozygotic twins, discordant for ulcerative colitis was selected. Illumina and Nimblegen platforms were used.

2012-09-27 | E-GEOD-27899 | biostudies-arrayexpress

Ulcerative Colitis subjects

Project description:Ulcerative Colitis subjects

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Gene Expression Profiling of Ulcerative Colitis

Project description:Through laser capture microdissection and microarray analysis combined with slightly modified RNA extraction and amplification. we could analyze the subtle differential expression between colon normal cell and ulcerative colitis. Keywords: Ulcerative Colitis, amplification, microdissection

2005-12-13 | GSE3801 | GEO

Transcription profiling of human ulcerative colitis colonic mucosa to define an ulcerative colitis preinflammatory state

Project description:The samples are a part of a study aiming at diagnosing ulcerative colitis from genome-wide gene expression analysis of the colonic mucosa. Colonic mucosal samples were collected as endoscopic pinch biopsies from ulcerative colitis patients and from control subjects. Samples with and without macroscopic signs of inflammation were collected from the patients. Experiment Overall Design: The series contain eight UC samples with macroscopic signs of inflammation, 13 UC smaples without macroscopic signs of inflammation, five control subjects.

2008-06-20 | E-GEOD-9452 | biostudies-arrayexpress

Project description:Hyperbaric Oxygen Therapy for Ulcerative Colitis

| PRJEB50260 | ENA

Hyperbaric Oxygen Promotes Both the Proliferation and Chemosensitization of Glioblastoma Cells by Inhibiting HIF1α/HIF2α-ABCG2

Project description:Hyperbaric oxygen enhances glioma chemosensitivity, but the mechanism remains unclear. Hypoxia is common in gliomas, and as the main effector molecules of hypoxia, HIF1α and HIF2α promote the malignant progression by inhibiting cell apoptosis and maintaining stemness. ABCG2 is a marker protein of tumor stem cells and drug efflux transporter protein. This study aims to reveal the detailed mechanism of hyperbaric oxygen promote both proliferation and chemosensitization. Under hyperbaric oxygen and hypoxic conditions, we investigated the differences in cell cycle, proliferation, apoptosis, LDH release, and the expression of proteins and mRNA. We also conducted studies on transcriptional regulation and performed in vivo experiments. It revealed that under hypoxic conditions, HIF1α, HIF2α, and ABCG2 are highly expressed, and both HIF1α and HIF2α promote ABCG2 expression. After hyperbaric oxygen treatment, the expression of HIF1α, HIF2α, and ABCG2 decreased, both cell proliferation and chemosensitivity increased. After knocking out HIF1α and HIF2α, cell proliferation and chemosensitivity increased, but the expression of stem cell marker proteins decreased. ChIP‒qPCR revealed that HIF1α and HIF2α target the ABCG2 promoter. Gain- and loss-of-function experiments suggested that ABCG2 can promote the expression of stem cell marker proteins, inhibit cell apoptosis, and promote tumor progression. This study confirmed that hyperbaric oxygen can inhibit ABCG2 expression through HIF1α and HIF2α, thereby promoting the proliferation and chemosensitization of gliomas.

2025-04-30 | GSE295278 | GEO

Methylation profiling in Ulcerative colitis

Project description:The series was designed to identify the different methylated single CpGs involved in the pathophysiology of ulcerative colitis.

2012-09-27 | GSE27899 | GEO

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