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Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [RNA-Seq]

ABSTRACT: Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [RNA-Seq]

PROVIDER: PRJNA1057260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27352400.fastq.gz	Fastqsanger.gz
	SRR27352401.fastq.gz	Fastqsanger.gz
	SRR27352402.fastq.gz	Fastqsanger.gz
	SRR27352403.fastq.gz	Fastqsanger.gz
	SRR27352404.fastq.gz	Fastqsanger.gz

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Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β

Project description:Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β

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Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [16S]

Project description:Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [16S]

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Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [16S]

Project description:Acute gastrointestinal infection with intracellular pathogens like Salmonella Typhimurium triggers the release of the proinflammatory cytokine interleukin 1β (IL-1β). However, the role of IL-1β in intestinal defense against Salmonella remains unclear. Here, we show that IL-1b production is detrimental during Salmonella infection. Mice lacking IL-1b (IL-1b -/-) failed to recruit neutrophils to the gut during infection, which reduced tissue damage and prevented depletion of short-chain fatty acid-producing commensals. Changes in epithelial cell metabolism that typically support pathogen expansion, such as switching energy production from fatty acid oxidation to fermentation, were absent in infected IL-1b -/- mice which inhibited Salmonella expansion. Additionally, we found that IL-1b induces expression of complement anaphylatoxins and suppresses the complement-inactivator Carboxypeptidase N (CPN1). Disrupting this process via IL-1b loss prevented mortality in Salmonella-infected IL-1b -/- mice. Finally, we found that IL-1b expression correlates with expression of the complement receptor in patients suffering from sepsis, but not uninfected patients and healthy individuals. Thus, Salmonella exploits IL-1b signaling to outcompete commensal microbes and establish gut colonization. Moreover, our findings identify the intersection of IL-1b signaling and the complement system as key host factors involved in controlling mortality during invasive Salmonellosis.

2024-01-08 | GSE252070 | GEO

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [RNA-Seq]

2024-01-08 | GSE252069 | GEO

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β.

Project description:Acute gastrointestinal infection with intracellular pathogens like Salmonella Typhimurium triggers the release of the proinflammatory cytokine interleukin 1β (IL-1β). However, the role of IL-1β in intestinal defense against Salmonella remains unclear. Here, we show that IL-1β production is detrimental during Salmonella infection. Mice lacking IL-1β (IL-1β -/-) failed to recruit neutrophils to the gut during infection, which reduced tissue damage and prevented depletion of short-chain fatty acid (SCFA)-producing commensals. Changes in epithelial cell metabolism that typically support pathogen expansion, such as switching energy production from fatty acid oxidation to fermentation, were absent in infected IL-1β -/- mice which inhibited Salmonella expansion. Additionally, we found that IL-1β induces expression of complement anaphylatoxins and suppresses the complement-inactivator carboxypeptidase N (CPN1). Disrupting this process via IL-1β loss prevented mortality in Salmonella-infected IL-1β -/- mice. Finally, we found that IL-1β expression correlates with expression of the complement receptor in patients suffering from sepsis, but not uninfected patients and healthy individuals. Thus, Salmonella exploits IL-1β signaling to outcompete commensal microbes and establish gut colonization. Moreover, our findings identify the intersection of IL-1β signaling and the complement system as key host factors involved in controlling mortality during invasive Salmonellosis.

| S-EPMC10826948 | biostudies-literature

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β

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

2024-01-08 | GSE252071 | GEO

Interleukin-1β effect on primary mouse articular chondrocytes

Project description:Gene expression profiling of primary mouse articular chondrocyte treated with interleukin-1β. In this study, we have attempted to explore the effects of interleukin-1β on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

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Interleukin-26 potentiates type 2 skin inflammation in presence of interleukin-1β

Project description:Interleukin-26 potentiates type 2 skin inflammation in presence of interleukin-1β

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Interleukin-1β effect on primary mouse articular chondrocytes

Project description:Interleukin-1β effect on primary mouse articular chondrocytes

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whole transcriptome map of osteoarthritic meniscus with or without interleukin-1β stimulation

Project description:We report the application of whole-transcriptome high throughput sequence on osteoarthritic degenerative meniscus with or without interleukin-1β stimulation. A total of 375 mRNAs, 15 miRNAs, 56 lncRNAs, and 90 circRNAs were significantly altered in the degenerative meniscus treated with IL-1β. qRT-PCR further revealed consistent expression pattern. More importantly, highly specific ceRNA networks regulated by lncRNA LOC107986251-miR-212-5p-SESN3 and hsa_circ_0018069-miR-147b-3p-TJP2 were identified during interleukin-induced meniscus degeneration.

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