ArticleJournal of leukocyte biology2012
IRF3 contributes to sepsis pathogenesis in the mouse cecal ligation and puncture model.
Article in Journal of leukocyte biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Sleep interruption aggravates sepsis by rewiring the macrophage immune response.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- A sinomenine derivative protects life-threatening inflammatory injuries via covalently binding to a novel allosteric inhibition site of IRF3.Acta pharmacologica Sinica · 2026Article
- IRF7 drives macrophages to kill bacteria and improves septic outcomes via autophagy.JCI insight · 2025Article
- CREATINE KINASE IS ELEVATED BY THE SUBMANDIBULAR VEIN BLEED TECHNIQUE, OBSCURING THE MEASUREMENT OF MUSCLE DAMAGE IN SEPSIS.Shock (Augusta, Ga.) · 2025Article
- Interferon Regulatory Factor 3 Exacerbates the Severity of COVID-19 in Mice.Critical care explorations · 2025Article
- IRF3 function and immunological gaps in sepsis.Frontiers in immunology · 2024Review
- Gut microbiota involved in leptospiral infections.The ISME journal · 2022Article
- STING1 in sepsis: Mechanisms, functions, and implications.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2022Review
- Low type I interferon response in COVID-19 patients: Interferon response may be a potential treatment for COVID-19.Biomedical reports · 2021Article
- IRF3 Signaling within the Mouse Stroma Influences Sepsis Pathogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway.Open medicine (Warsaw, Poland) · 2021Article
- Aged IRF3-KO Mice are Protected from Sepsis.Journal of inflammation research · 2021Article
- Fecal microbiota transplant rescues mice from human pathogen mediated sepsis by restoring systemic immunity.Nature communications · 2020Article
- STING-mediated intestinal barrier dysfunction contributes to lethal sepsis.EBioMedicine · 2019Article
- LDK378 improves micro- and macro-circulation via alleviating STING-mediated inflammatory injury in a Sepsis rat model induced by Cecal ligation and puncture.Journal of inflammation (London, England) · 2019Article
- Circadian Rhythms Influence the Severity of Sepsis in Mice via a TLR2-Dependent, Leukocyte-Intrinsic Mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Poly(I:C) Priming Exacerbates Cecal Ligation and Puncture-Induced Polymicrobial Sepsis in Mice.Inflammation · 2018Article
- IRF3 Inhibits Neutrophil Recruitment in Mice Infected with Pseudomonas aeruginosa.Inflammation · 2017Article
- Splenic RNA and MicroRNA Mimics Promote Complement Factor B Production and Alternative Pathway Activation via Innate Immune Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Acute-Phase Deaths from Murine Polymicrobial Sepsis Are Characterized by Innate Immune Suppression Rather Than Exhaustion.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Much remains to be learned regarding which components of the innate immune response are protective versus detrimental during sepsis. Prior reports demonstrated that TLR9 and MyD88 play key roles in the CLP mouse model of sepsis; however, the role of additional PRRs and their signaling intermediates remains to be explored. In a prior report, we demonstrated that the signal adaptor IRF3 contributes to the systemic inflammatory response to liposome:DNA. We hypothesized that IRF3 might likewise promote sepsis in the CLP model. Here, we present results demonstrating that IRF3-KO mice have reduced disease score, mortality, hypothermia, and bacterial load following CLP versus WT counterparts. This is paired with reduced levels of systemic inflammatory mediators in IRF3-KO mice that undergo CLP. We demonstrate that peritoneal cells from WT CLP mice produce more cytokines than IRF3-KO counterparts on a per-cell basis; however, there are more cells in the peritoneum of IRF3-KO CLP mice. Finally, we show that IRF3 is activated in macrophages cultured with live or sonicated commensal bacteria. These results demonstrate that IRF3 plays a detrimental role in this mouse model of sepsis.
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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.