ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Interruption of macrophage-derived IL-27(p28) production by IL-10 during sepsis requires STAT3 but not SOCS3.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- Discordant Interleukin-27 (IL-27) Subunit Transcription in Human Sepsis Exposes a Molecular-Attribution Gap.Biomedicines · 2026Article
- IL-27 neutralization with and without antibiotics as an approach to prevent and treat neonatal sepsis.JCI insight · 2026Article
- Proton-activated chloride channel 1 is essential for innate host defense against bacterial sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- IL-12 family cytokines and autoimmune diseases: A potential therapeutic target?Journal of translational autoimmunity · 2025Review
- Gut microbiota-derived acetic acids promoted sepsis-induced acute respiratory distress syndrome by delaying neutrophil apoptosis through FABP4.Cellular and molecular life sciences : CMLS · 2024Article
- Externalized histones fuel pulmonary fibrosis via a platelet-macrophage circuit of TGFβ1 and IL-27.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- IL-30 protects against sepsis-induced myocardial dysfunction by inhibiting pro-inflammatory macrophage polarization and pyroptosis.iScience · 2023Article
- CD11a regulates hematopoietic stem and progenitor cells.Frontiers in immunology · 2023Article
- IL-27 Enhances γδ T Cell-Mediated Innate Resistance to Primary Hookworm Infection in the Lungs.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Exosomes from adipose-derived mesenchymal stem cells alleviate sepsis-induced lung injury in mice by inhibiting the secretion of IL-27 in macrophages.Cell death discovery · 2022Article
- IL27 gene expression distinguishes multisystem inflammatory syndrome in children from febrile illness in a South African cohort.Frontiers in immunology · 2022Article
- Bacterial polyphosphates induce CXCL4 and synergize with complement anaphylatoxin C5a in lung injury.Frontiers in immunology · 2022Article
- [Research advances on the regulation of interleukin-17 signal transduction and the implication of interleukin-17 in sepsis].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Review
- The IL-27 receptor regulates TIGIT on memory CD4iScience · 2021Article
- Interleukin-27 and Its Diverse Effects on Bacterial Infections.Frontiers in immunology · 2021Review
- JAK/STAT signaling pathway-mediated microRNA-181b promoted blood-brain barrier impairment by targeting sphingosine-1-phosphate receptor 1 in septic rats.Annals of translational medicine · 2020Article
- Bacterial polyphosphates interfere with the innate host defense to infection.Nature communications · 2020Article
- IL-27 regulation of innate immunity and control of microbial growth.Future science OA · 2020Review
- Elevated Levels of Interleukin-27 in Early Life Compromise Protective Immunity in a Mouse Model of Gram-Negative Neonatal Sepsis.Infection and immunity · 2020Article
- Neutrophil extracellular traps impair fungal clearance in a mouse model of invasive pulmonary aspergillosis.Immunobiology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/6 mice during sepsis. Genetic disruption of IL-27 signaling enhanced the respiratory burst of macrophages. Experiments using splenectomized mice or treatment with clodronate liposomes suggested that macrophages in the spleen may be a significant source of IL-27(p28) during sepsis. In cultures of TLR4-activated macrophages, the frequency of F4/80(+)CD11b(+)IL-27(p28)(+) cells was reduced by the addition of IL-10. IL-10 antagonized both MyD88-dependent and TRIF-dependent release of IL-27(p28). Genetic deletion of STAT3 in Tie2-Cre/STAT3flox macrophages completely interrupted the inhibition of IL-27(p28) by IL-10 after TLR4 activation. In contrast, IL-10 remained fully active to suppress IL-27(p28) with deletion of SOCS3 in Tie2-Cre/SOCS3flox macrophages. Blockade of IL-10R by Ab or genetic deficiency of IL-10 resulted in 3-5-fold higher concentrations of IL-27(p28) in endotoxic shock and polymicrobial sepsis. Our studies identify IL-10 as a critical suppressing factor for IL-27(p28) production during infection-associated inflammation. These findings may be helpful for a beneficial manipulation of adverse IL-27(p28) release during sepsis.
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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.