ArticleInternational dental journal2026
Recombinant IL-38 Alleviates Temporomandibular Joint Synovial Inflammation via IL-1R1-NF-κB-IL1β Pathway.
Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
INTRODUCTION AND
aimsInterleukin (IL)-38 has been identified as an anti-inflammatory cytokine; however, its specific role in temporomandibular joint (TMJ) synovial inflammation and the identity of its functional receptors remain elusive. This study aimed to investigate the therapeutic efficacy of IL-38 in TMJ synovial inflammation and to elucidate its potential receptor mechanisms.
methodsA rat model of temporomandibular joint osteoarthritis (TMJOA) was established via bilateral TMJ injection of mono-iodoacetate (MIA). Fifteen Sprague-Dawley (SD) rats were randomly allocated into three groups: sham (PBS), model (MIA), and treatment (MIA +human recombinant IL-38, hIL-38). Protein BLAST analysis was utilized to predict IL-38 function and receptor affinity. Synovial histopathology was assessed using HE staining. Quantitative real-time PCR (qPCR) was employed to quantify inflammatory gene expression, while immunohistochemistry (IHC) was utilized to detect inflammatory proteins and IL-1 receptor type 1 (IL-1R1) expression. Protein-protein interaction (PPI) network and protein-protein docking analyses were performed to predict the interaction between IL-38 and IL-1R1.
resultsIL-38 exhibited 43% identity and 55% positivity with interleukin-1 receptor antagonist (IL-1Ra), its precursor, and its isoforms X1 and X2. HE staining demonstrated that hIL-38 significantly reduced synovial inflammatory cell infiltration. IHC staining revealed that hIL-38 inhibited macrophage infiltration (CD68⁺) and suppressed the expression of iNOS and COX-2, thereby attenuating synovial inflammation. Docking and PPI analyses corroborated a direct interaction between IL-38 and IL-1R1. Furthermore, IHC staining indicated that IL-38 down-regulated the protein levels of IL-1R1, NF-κB p65, and IL-1β.
conclusionsIL-38 functions as a novel anti-inflammatory cytokine that alleviates TMJ synovial inflammation, potentially by antagonizing IL-1R1 and blocking the NF-κB signalling cascade. CLINICAL RELEVANCE: IL-38 may offer a novel therapeutic strategy for alleviating synovial inflammation in TMJOA.
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