ArticleLaboratory investigation; a journal of technical methods and pathology2019
IL-1α and IL-1β promote NOD2-induced immune responses by enhancing MAPK signaling.
Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
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- Anti-inflammatory effects of amarogentin on 2,4-dinitrochlorobenzene-induced atopic dermatitis-like mice and in HaCat cells.Animal models and experimental medicine · 2023Article
- Transcriptome alterations in chicken HD11 cells with steady knockdown and overexpression of RIPK2 gene.Poultry science · 2023Article
- IL-1β promotes A7r5 and HASMC migration and invasion via the p38-MAPK/Angpt-2 pathway.European journal of medical research · 2022Article
- IL-1 and autoinflammatory disease: biology, pathogenesis and therapeutic targeting.Nature reviews. Rheumatology · 2022Review
- NOD2 is involved in regulating odontogenic differentiation of DPSCs suppressed by MDP through NF-κB/p65 signaling.Cytotechnology · 2022Article
- Interference of Interleukin-1Mediators of inflammation · 2022Article
- Expression of Peripheral Blood DCs CD86, CD80, and Th1/Th2 in Sepsis Patients and Their Value on Survival Prediction.Computational and mathematical methods in medicine · 2022Article
- Curcumin-primed human BMSC-derived extracellular vesicles reverse IL-1β-induced catabolic responses of OA chondrocytes by upregulating miR-126-3p.Stem cell research & therapy · 2021Article
- Downregulation of NUDT21 contributes to cervical cancer progression through alternative polyadenylation.Oncogene · 2021Article
- Identification of the Crucial Gene in Overflow Arteriovenous Fistula by Bioinformatics Analysis.Frontiers in physiology · 2021Article
- Transport Stress Induces Skin Innate Immunity Response in Hybrid Yellow Catfish (Frontiers in immunology · 2021Article
- Limonin Inhibits IL-1Oxidative medicine and cellular longevity · 2021Article
- NOD1/RIP2 signalling enhances the microglia-driven inflammatory response and undergoes crosstalk with inflammatory cytokines to exacerbate brain damage following intracerebral haemorrhage in mice.Journal of neuroinflammation · 2020Article
- Negative feedback loop of ERK/CREB/miR-212-3p inhibits HBeAg-induced macrophage activation.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) induce a tightly regulated inflammatory response at risk of causing tissue damage, depending on the effectiveness of ensuing negative feedback regulatory mechanisms. Cross-regulation between TLRs, NLRs, and cytokine receptors has been observed. However, the cross-regulation between interleukin-1 (IL-1) receptors and NOD2 is not completely understood. In this study, we found that IL-1α/β increased NOD2-induced inflammatory response in human monocytic THP1 cells, peripheral blood mononuclear cells (PBMCs), mouse macrophage RWA264.7 cells and spleen cells, and in an in vivo experiment. IL-1α/β pre-treatment induced the production of CXC chemokines, including growth-regulated oncogene (GRO)-α, GRO-β, and IL-8, and proinflammatory cytokines, including IL-1β, IL-6, and TNFα, which are induced by the activation of NOD2, in a dose- and time-dependent manner. However, pre-treatment with the NOD2 ligand muramyl dipeptide (MDP) did not up-regulate the expression of cytokines induced by IL-1α/β re-treatment. IL-1β treatment increased the expression of A20, which is an important inhibitor of the innate immune response. However, the overexpression of A20 failed to inhibit MDP-induced cytokine production, suggesting that A20 had no effects on the NOD2-induced immune response. In addition, IL-1α/β increased the expression of NOD2 and its downstream adaptor RIP2, and IL-1α/β pre-treatment increased MDP-induced activation of mitogen-activated protein kinases (MAPKs), including ERK, JNK, and P38, which contributed to MDP-induced cytokine production. Based on these results, IL-1α/β promote the NOD2-induced immune responses by enhancing MDP-induced activation of MAPK signaling pathways.
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