ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Salmonella Typhimurium Co-Opts the Host Type I IFN System To Restrict Macrophage Innate Immune Transcriptional Responses Selectively.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 64 citations in OpenAlex.
- Salmonella infection and biofilms drive anti-C1q and anti-dsDNA autoantibodies in systemic autoimmunity.PLoS pathogens · 2026Article
- Contribution of localmBio · 2026Article
- EnhancedInfection and immunity · 2026Article
- By dawn or dusk-how circadian timing rewrites bacterial infection outcomes.FEBS letters · 2026Review
- Targeted Lipid Metabolism Screening Uncovers Regulatory Effects on the STING Immune Response in Mevalonate, Eicosanoid and Fatty Acid Pathways.bioRxiv : the preprint server for biology · 2026Article
- Targeted lipid metabolism screening uncovers regulatory effects on the STING immune response in mevalonate, eicosanoid and fatty acid pathways.Frontiers in immunology · 2026Article
- Temporal dynamics of macrophage activation duringVirulence · 2025Article
- Single-cell analysis of genetically minimized Salmonella reveals effector gene cooperation in vivo.Nature microbiology · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Genome-wide identification of the interferon complex establishes IFNf in Cypriniformes.BMC biology · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Article
- ER-transiting bacterial toxins amplify STING innate immune responses and elicit ER stress.Infection and immunity · 2024Article
- Article
- Disulfiram ameliorates STING/MITA-dependent inflammation and autoimmunity by targeting RNF115.Cellular & molecular immunology · 2024Article
- Establishment of aJournal of pathogens · 2024Article
- Mycobacterium tuberculosis SecA2-dependent activation of host Rig-I/MAVs signaling is not conserved in Mycobacterium marinum.PloS one · 2024Article
- LNCGM1082-mediated NLRC4 activation drives resistance to bacterial infection.Cellular & molecular immunology · 2023Article
- Proteomics Profiling Reveals Regulation of Immune Response to Salmonella enterica Serovar Typhimurium Infection in Mice.Infection and immunity · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Innate immune inflammatory responses are subject to complex layers of negative regulation at intestinal mucosal surfaces. Although the type I IFN system is critical for amplifying antiviral immunity, it has been shown to play a homeostatic role in some models of autoimmune inflammation. Type I IFN is triggered in the gut by select bacterial pathogens, but whether and how the type I IFN might regulate innate immunity in the intestinal environment have not been investigated in the context of Salmonella enterica serovar Typhimurium (ST). ST infection of human or murine macrophages reveals that IFN-β selectively restricts the transcriptional responses mediated by both the TLRs and the NOD-like receptors. Specifically, IFN-β potently represses ST-dependent innate induction of IL-1 family cytokines and neutrophil chemokines. This IFN-β-mediated transcriptional repression was independent of the effects of IFN-β on ST-induced macrophage cell death, but significantly dependent on IL-10 regulation. We further evaluated ST pathogenesis in vivo following oral inoculation of mice lacking IFN-β. We show that IFN-β(-/-) mice exhibit greater resistance to oral ST infection and a slower spread of ST to distal sterile sites. This work provides mechanistic insight into the relationship between ST and type I IFN, and demonstrates an additional mechanism by which IFN-β may promote spread of enteric pathogens.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.