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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE166038 | GEO | 2021/11/24

REPOSITORIES: GEO

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

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 | GSE166030 | GEO

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

Project description: Not available

| S-EPMC8600093 | biostudies-literature

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

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

| PRJNA699006 | ENA

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 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 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

Lactobacillus rhamnosus GG modifies the metabolome of pathobionts in gnotobiotic mice

Project description:Lactobacillus rhamnosus GG (LGG) is the most widely used probiotic, but the mechanisms underlying its beneficial effects remain unresolved. Previous studies typically inoculated LGG in hosts with established gut microbiota, limiting the understanding of specific impacts of LGG on host due to numerous interactions among LGG, commensal microbes, and the host. There has been a scarcity of studies that used gnotobiotic animals to elucidate LGG-host interaction, in particular for gaining specific insights about how it modifies metabolome. To evaluate whether LGG affects the metabolite output of pathobionts, we inoculated LGG into gnotobiotic mice along with a gut-disruptive consortium containing Propionibacterium acnes, Turicibacter sanguinis, and Staphylococcus aureus (PTS).

2020-08-07 | MSV000085927 | MassIVE

A Pathobiont of the Microbiota Balances Host Colonization and Intestinal Inflammation

Project description:The mammalian gastrointestinal tract harbors a diverse microbiota residing in intimate contact with the host immune system. Though most associations are symbiotic or commensal, some resident bacteria (termed pathobionts) have the potential to induce disease in immunocompromised hosts. Type VI secretion systems (T6SSs) have recently emerged as a novel mechanism for forging microbial-host interactions during infection. We reveal here a unique protective role for the T6SS of Helicobacter hepaticus, a Gram-negative bacterium of the murine intestinal microbiota. The T6SS of H. hepaticus targets effector substrates to intestinal epithelial cells (IECs). Mutants in T6SSs display higher intracellular and cell-associated numbers upon incubation with IECs, and exhibit increased bacterial colonization of the gastrointestinal tract compared to wild-type bacteria. The T6SS accordingly directs an anti-inflammatory gene expression profile in IECs co-cultured with H. hepaticus. Remarkably, T6SS mutants induce an exacerbated pro-inflammatory response in an experimental model of colitis. CD4+ T cells isolated from T6SS mutant-colonized animals produce increased T-helper 17 (Th17) cytokines in response to IECs presenting H. hepaticus antigens. These data demonstrate that H. hepaticus intimately interacts with IECs and employs type VI secretion to establish a balanced host relationship by limiting microbial colonization and intestinal inflammation. We propose that altering host-bacterial equilibriums that lead to dysbiosis of the microbiota contributes to human disorders such as inflammatory bowel disease and colon cancer.

2010-06-01 | GSE20434 | GEO

Cross-feeding between intestinal pathobionts promotes their overgrowth during undernutrition

Project description:Child undernutrition is a global health issue associated with a high burden of infectious disease. Undernourished children display an overabundance of intestinal pathogens and pathobionts, and these bacteria induce enteric dysfunction in undernourished mice; however, the cause of their overgrowth remains poorly defined. Here, we show that disease-inducing human isolates of Enterobacteriaceae and Bacteroidales spp. are capable of multi-species symbiotic cross-feeding, resulting in synergistic growth of a mixed community in vitro. Growth synergy occurs uniquely under malnourished conditions limited in protein and iron: in this context, Bacteroidales spp. liberate diet- and mucin-derived sugars and Enterobacteriaceae spp. enhance the bioavailability of iron. Analysis of human microbiota datasets reveals that Bacteroidaceae and Enterobacteriaceae are strongly correlated in undernourished children, but not in adequately nourished children, consistent with a diet-dependent growth synergy in the human gut. Together these data suggest that dietary cross-feeding fuels the overgrowth of pathobionts in undernutrition.

2021-07-11 | ST001862 | MetabolomicsWorkbench

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