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SRX23028990: GSM7993285: WT d2 #2; Mus musculus; RNA-Seq
4 ILLUMINA (NextSeq 550) runs: 18.8M spots, 1.4G bases, 572.8Mb downloads

External Id: GSM7993285_r1
Submitted by: The Azrieli Faculty of Medicine, Bar-Ilan University
Study: Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1ß [RNA-Seq]
show Abstracthide Abstract
Acute gastrointestinal infection with intracellular pathogens like Salmonella Typhimurium triggers the release of the proinflammatory cytokine interleukin 1ß (IL-1ß). However, the role of IL-1ß 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. Overall design: WT and IL-1b-/- C57BL/6 mice were orally infected with 10^7 CFU of Salmonella typhimurium SL1334. Colonic tissues were removed at 2 and 6 days post infection and RNA was exptracted and sequenced.
Sample: WT d2 #2
SAMN39127996 • SRS19990874 • All experiments • All runs
Organism: Mus musculus
Library:
Name: GSM7993285
Instrument: NextSeq 550
Strategy: RNA-Seq
Source: TRANSCRIPTOMIC
Selection: cDNA
Layout: SINGLE
Construction protocol: RNA from frozen colonic tissues was extracted using Qiagen RNeasy Universal kit. Integrity of the isolated RNA was analysed using the Agilent TS HS RNA Kit and TapeStation 4200 1000ng of total RNA was treated with the NEBNext poly (A) mRNA Magnetic Isolation Module (NEB, #E7490L). RNA sequencing libraries were produced by using the NEBNext Ultra II RNA Library Prep Kit for Illumina (NEB #E7770L). Quantification of the library was performed using a dsDNA HS Assay Kit and Qubit (Molecular Probes, Life Technologies) and qualification was done using the Agilent TS D1000 kit and TapeStation 4200. 250nM of each library was pooled together and diluted to 4nM according to the NextSeq manufacturer's instructions. 1.6pM was loaded onto the Flow Cell with 1% PhiX library control. Libraries were sequenced with the Illumina NextSeq 550 platform with single-end reads of 75 cycles according to the manufacturer's instructions.
Runs: 4 runs, 18.8M spots, 1.4G bases, 572.8Mb
Run# of Spots# of BasesSizePublished
SRR273524114,744,820353.4M143.6Mb2024-01-08
SRR273524124,644,988345.9M139.4Mb2024-01-08
SRR273524134,766,676355M147.6Mb2024-01-08
SRR273524144,622,229344.3M142.2Mb2024-01-08

ID:
31108599

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