ArticleJournal of leukocyte biology2017
IL-23 restoration of Th17 effector function is independent of IL-6 and TGF-β in a mouse model of alcohol and burn injury.
Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Role of oxidative stress in post-burn wound healing.Burns & trauma · 2025Review
- IL-23 Promotes Neutrophil Extracellular Trap Formation and Bacterial Clearance in a Mouse Model of Alcohol and Burn Injury.ImmunoHorizons · 2022Article
- Deciphering the endometrial immune landscape of RIF during the window of implantation from cellular senescence by integrated bioinformatics analysis and machine learning.Frontiers in immunology · 2022Article
- 6-Formylindolo (3, 2-b) Carbazole (FICZ)-mediated protection of gut barrier is dependent on T cells in a mouse model of alcohol combined with burn injury.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Autotaxin-Lysophosphatidic Acid Axis Blockade Improves Inflammation by Regulating Th17 Cell Differentiation in DSS-Induced Chronic Colitis Mice.Inflammation · 2019Article
- The Comparative Study of the Therapeutic Effects and Mechanism of Baicalin, Baicalein, and Their Combination on Ulcerative Colitis Rat.Frontiers in pharmacology · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
T cells play a critical role in host defense against intestinal bacteria. We have shown that ethanol combined with burn injury suppresses Peyer's patch (PP) Th17 cytokines 1 d after injury. We assessed the mechanism of suppressed Th17 effector functions. Mice were gavaged with ethanol 4 h before burn injury and euthanized 1, 3, and 7 d after injury. Mesenteric lymph nodes (MLNs), PPs, and spleen Th1 and Th17 cytokines were assessed. A significant decrease in IL-17, IL-22, IL-2, and IFN-γ were observed in all 3 lymphoid organs 1 and 3 d after injury. We used splenic cells to study the role of IL-6, IL-23, TGF-β, and aryl hydrocarbon receptor (AHR) in suppressing Th17 cytokines. We also assessed whether the AHR agonist 6-formylindolo (3, 2-b) carbazole (FICZ) modulates Th17 cytokines. We found a significant decrease in IL-6 and TGF-β after ethanol and burn; IL-23 was undetectable. The reconstitution of IL-23 in culture medium increased IL-17 by 2-fold and IL-22 by 20-fold in cells from burn ethanol mice. The restoration of IL-6 and TGF-β combined did not influence the release of Th17 cytokines. We observed that AHR was necessary for IL-23 restoration of IL-22 after ethanol and burn injury. The AHR agonist FICZ enhanced IL-22, but not IL-17. None of these treatments influenced the release of Th1 cytokines. Together, these results suggest that IL-23 plays a critical role in regulation of Th17 cytokines. Furthermore, IL-6 and TGF-β do not appear to influence IL-23-mediated restoration of Th17 cytokines after ethanol and burn injury.
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