ArticlePloS one2012
IL-36α exerts pro-inflammatory effects in the lungs of mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The trial behind it
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Who cites it
49 citing papers in PubMed, 113 citations in OpenAlex.
- High Expression of IL-36γ in Influenza Patients Regulates Interferon Signaling Pathway and Causes Programmed Cell Death During Influenza Virus Infection.Frontiers in immunology · 2020Trial
- IL-36 activates neutrophil extracellular traps and exacerbates LPS-induced ARDS in mice.Scientific reports · 2026Article
- Mucosal IL-36 is a defining feature of severe paediatric bronchiolitis.Mucosal immunology · 2026Article
- The role of IL-18 and IL-33 in the bronchoalveolar lavage fluid of children with severe community-acquired pneumonia complicated with pleural effusion.Frontiers in pediatrics · 2025Article
- FloxedCells · 2024Article
- Different expression levels of interleukin-36 in asthma phenotypes.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024Article
- Interleukin-36 is overexpressed in human sepsis and IL-36 receptor deletion aggravates lung injury and mortality through epithelial cells and fibroblasts in experimental murine sepsis.Critical care (London, England) · 2023Article
- IL-36α inhibits melanoma by inducing pro-inflammatory polarization of macrophages.Cancer immunology, immunotherapy : CII · 2023Article
- IL-36 receptor agonist and antagonist imbalance drives neutrophilic inflammation in COPD.JCI insight · 2022Article
- IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic.Frontiers in immunology · 2022Review
- Glucose Homeostasis in Relation to Neutrophil Mobilization in Smokers with COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- NSC828779 Alleviates Renal Tubulointerstitial Lesions Involving Interleukin-36 Signaling in Mice.Cells · 2021Article
- IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore.Cellular and molecular life sciences : CMLS · 2021Review
- IL-36α Exerts Proinflammatory Effects in Aspergillus fumigatus Keratitis of Mice Through the Pathway of IL-36α/IL-36R/NF-κB.Investigative ophthalmology & visual science · 2021Article
- IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice.Communications biology · 2021Article
- Walking down the "IL": The Newfound Marriage between IL-36 and Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2021Article
- IL-36 Cytokines Promote Inflammation in the Lungs of Long-Term Smokers.American journal of respiratory cell and molecular biology · 2021Article
- IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021Review
- Interleukin-38 ameliorates poly(I:C) induced lung inflammation: therapeutic implications in respiratory viral infections.Cell death & disease · 2021Article
- The Pre-Implantation Embryo Induces Uterine Inflammatory Reaction in Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Interleukin (IL-) 36 cytokines (previously designated as novel IL-1 family member cytokines; IL-1F5- IL-1F10) constitute a novel cluster of cytokines structurally and functionally similar to members of the IL-1 cytokine cluster. The effects of IL-36 cytokines in inflammatory lung disorders remains poorly understood. The current study sought to investigate the effects of IL-36α (IL-1F6) and test the hypothesis that IL-36α acts as a pro-inflammatory cytokine in the lung in vivo. Intratracheal instillation of recombinant mouse IL-36α induced neutrophil influx in the lungs of wild-type C57BL/6 mice and IL-1αβ(-/-) mice in vivo. IL-36α induced neutrophil influx was also associated with increased mRNA expression of neutrophil-specific chemokines CXCL1 and CXCL2 in the lungs of C57BL/6 and IL-1αβ(-/-) mice in vivo. In addition, intratracheal instillation of IL-36α enhanced mRNA expression of its receptor IL-36R in the lungs of C57BL/6 as well as IL-1αβ(-/-) mice in vivo. Furthermore, in vitro incubation of CD11c(+) cells with IL-36α resulted in the generation of neutrophil-specific chemokines CXCL1, CXCL2 as well as TNFα. IL-36α increased the expression of the co-stimulatory molecule CD40 and enhanced the ability of CD11c(+) cells to induce CD4(+) T cell proliferation in vitro. Furthermore, stimulation with IL-36α activated NF-κB in a mouse macrophage cell line. These results demonstrate that IL-36α acts as a pro-inflammatory cytokine in the lung without the contribution of IL-1α and IL-1β. The current study describes the pro-inflammatory effects of IL-36α in the lung, demonstrates the functional redundancy of IL-36α with other agonist cytokines in the IL-1 and IL-36 cytokine cluster, and suggests that therapeutic targeting of IL-36 cytokines could be beneficial in inflammatory lung diseases.
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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.