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Gut commensal bacteria enhance pathogenesis of a tumorigenic murine retrovirus

ABSTRACT: Gut commensal bacteria enhance pathogenesis of a tumorigenic murine retrovirus

PROVIDER: PRJNA862347 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20648442.fastq.gz	Fastqsanger.gz
	SRR20648443.fastq.gz	Fastqsanger.gz
	SRR20648444.fastq.gz	Fastqsanger.gz
	SRR20648445.fastq.gz	Fastqsanger.gz
	SRR20648446.fastq.gz	Fastqsanger.gz

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Gut commensal bacteria enhance pathogenesis of a tumorigenic murine retrovirus

Project description:The influence of the microbiota on viral transmission and replication is well appreciated. However, its impact on retroviral pathogenesis outside of transmission/replication control remained unknown. Using Murine Leukemia Virus (MuLV), we found that some commensal bacteria promoted the development of leukemia induced by this retrovirus. The promotion of leukemia development by commensals was due to suppression of the adaptive immune response through upregulation of several negative regulators of immunity. These negative regulators included Serpinb9b and Rnf128, which are associated with a poor prognosis of some spontaneous human cancers. Upregulation of Serpinb9b was mediated by sensing of bacteria by NOD1/NOD2/RIPK2 pathway. This work describes a novel mechanism by which the microbiota enhances tumorigenesis within gut-distant organs and points at potential new targets for cancer therapy.

2022-07-29 | GSE209752 | GEO

Gut commensal bacteria enhance pathogenesis of a tumorigenic murine retrovirus.

Project description:The influence of the microbiota on viral transmission and replication is well appreciated. However, its impact on retroviral pathogenesis outside of transmission/replication control remains unknown. Using murine leukemia virus (MuLV), we found that some commensal bacteria promoted the development of leukemia induced by this retrovirus. The promotion of leukemia development by commensals is due to suppression of the adaptive immune response through upregulation of several negative regulators of immunity. These negative regulators include Serpinb9b and Rnf128, which are associated with a poor prognosis of some spontaneous human cancers. Upregulation of Serpinb9b is mediated by sensing of bacteria by the NOD1/NOD2/RIPK2 pathway. This work describes a mechanism by which the microbiota enhances tumorigenesis within gut-distant organs and points at potential targets for cancer therapy.

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Project description:Clostridioides difficile is one of the most common nosocomial pathogens and a global public health threat. Upon colonization of the gastrointestinal tract, C. difficile is exposed to a rapidly changing polymicrobial environment and a dynamic metabolic milieu. Despite the link between the gut microbiota and susceptibility to C. difficile, the impact of synergistic interactions between the microbiota and pathogens on the outcome of infection is largely unknown. Here, we show that microbial cooperation between C. difficile and Enterococcus has a profound impact on the growth, metabolism, and pathogenesis of C. difficile.. Through a process of nutrient restriction and metabolite cross-feeding, E. faecalis shapes the metabolic environment in the gut to enhance C. difficile fitness and increase toxin production. These findings demonstrate that members of the microbiota, such as Enterococcus, have a previously unappreciated impact on C. difficile behavior and virulence.

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Project description:The microbiota plays a fundamental role in regulating host immunity. However, the processes that initiate homeostatic immunity to the microbiota remain largely unknown. Here, we show that the skin microbiota promotes the discrete expression of defined endogenous retrovirus (ERVs). Keratinocyte-intrinsic responses to ERVs depended on cGAS/STING signaling and promoted the induction commensal specific T cells including CD8+, CD4+ and MAIT cells. Inhibition of reverse transcriptase significantly impacted these responses resulting in impaired homeostatic immunity to the microbiota and associated tissue repair function. Conversely, diets that caused an increase in dietary lipids primed the skin for aberrant ERV expression in response to commensal colonization, leading to tissue inflammation. Together, our results support the idea that the host may have coopted its endogenous virome as a means to communicate with the exogenous microbial microbiota, resulting in a multikingdom dialogue that controls both tissue homeostasis and inflammation.

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2019-09-03 | E-MTAB-6774 | biostudies-arrayexpress

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