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Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses

ABSTRACT: Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses

PROVIDER: PRJNA699006 | ENA |

REPOSITORIES: ENA

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Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses A

Project description:Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses A

| PRJNA699003 | ENA

Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses B

Project description:Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses B

| PRJNA699013 | ENA

Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses B

Project description:Microbiota dysbiosis and mucosa-associated bacteria are involved in colorectal cancer progression. We hypothesized that a time-specific interaction between dysbiotic pathobionts and host responses promote tumor growth. This study aimed to elucidate the dysfunctional host-microbe interplay in colon tumorigenesis by using a time-series metagenomics approach. A transient surge in fecal microbial richness was linked to a unique transcriptome profile in the mouse colon during carcinoma transformation. Monitoring gut microbiome may help identifying the window-of-opportunity to induce tumor regression using bacteria-targeted precision medicine.

2021-11-24 | GSE166038 | GEO

Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses A

2021-11-24 | GSE166030 | GEO

Invasive pathobionts in intestinal microbiome contributes to cancer initiation by counterbalancing epithelial antimicrobial responses

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-24 | GSE166039 | GEO

Invasive Pathobionts Contribute to Colon Cancer Initiation by Counterbalancing Epithelial Antimicrobial Responses.

Project description: Not available

| S-EPMC8600093 | biostudies-literature

Extracellular traps released by antimicrobial TH17 cells contributes to host defense

Project description:Herein, we used C. acnes as a model to elucidate the antimicrobial machinery of the TH17 subset. We generated C. acnes-specific antimicrobial TH17 clones (AMTH17) with varying antimicrobial activity against C. acnes, to enable us to study mechanisms by which TH17 cells kill bacteria. We show that C. acnes-induced AMTH17 clones represent a subset of CD4+ TEM and TEMRA cells. RNA-seq analysis of AMTH17 indicate transcripts encoding antimicrobial molecules such as GNLY, GZMB, PRF1 and histone H2B, whose expression correlates with killing activity. Additionally, we validated that AMTH17-mediated killing is a general mechanism that can target C. acnes and other bacterial species. Scanning electron microscopy reveal that AMTH17s can release T cell extracellular traps composed of lysine and arginine-rich histones such as H2B and H4 that entangle C. acnes. This study identifies a functionally distinct subpopulation of TH17 cells with an ability to secrete antimicrobial proteins and form extracellular T cell traps to capture and kill bacteria.

2021-12-01 | GSE144852 | GEO

Extracellular traps released by antimicrobial TH17 cells contributes to host defense

Project description:Extracellular traps released by antimicrobial TH17 cells contributes to host defense

| PRJNA605152 | ENA

Invasive Escherichia coli contributes to colon carcinogenesis by suppressing epithelial autophagy: application of phage therapy

Project description:Microbiota dysbiosis and mucosa-associated bacteria are involved in colorectal cancer (CRC) progression. However, the temporal changes in commensal-derived pathobionts and host-microbe interactions remain poorly understood. Our study demonstrated that antibiotic (ABX) treatment at a mid phase but not at early or late time points reduced tumor burden in a chemically induced CRC mouse model. A transient surge in fecal microbial richness and emergence of virulence factors were observed at the mid phase of CRC induction. Mouse colonic mucosal tissues were collected before (day 0) and on various days after administration of AOM/DSS (i.e., day 46 as early phase, day 56 as mid phase, and day 66 as late phase), and were analyzed using microarray. Unique profiles of autophagy-related genes were identified in the colonic mucosa during the mid phase, which correlated with the presence of intraepithelial bacteria.

2021-11-24 | GSE144719 | GEO

Keystone pathobionts associated with colorectal cancer promote oncogenic reprograming

Project description:Fusobacterium nucleatum (Fn) and enterotoxigenic Bacteroides fragilis (ETBF) are two pathobionts consistently enriched in the gut microbiomes of patients with CRC compared to healthy counterparts and frequently observed for their direct association within tumors. Although several molecular mechanisms have been identified that directly link these organisms to features of CRC in specific cell types, their specific effects on the epithelium and local immune compartment are not well-understood. To fill this gap, we leveraged single-cell RNA sequencing (scRNA-seq) on wildtype mice and mouse model of CRC. We find that Fn and ETBF exacerbate cancer-like transcriptional phenotypes in transit-amplifying and mature enterocytes in a mouse model of CRC. We also observed increased T cells in the pathobiont-exposed mice, but these pathobiont-specific differences observed in wildtype mice were abrogated in the mouse model of CRC. Although there are similarities in the responses provoked by each organism, we find pathobiont-specific effects in Myc-signaling and fatty acid metabolism. These findings support a role for Fn and ETBF in potentiating tumorigenesis via the induction of a cancer stem cell-like transit-amplifying and enterocyte population and the disruption of CTL cytotoxic function.

2024-01-19 | GSE220136 | GEO

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