ArticleThe Journal of biological chemistry2015
IL-1R/TLR2 through MyD88 Divergently Modulates Osteoclastogenesis through Regulation of Nuclear Factor of Activated T Cells c1 (NFATc1) and B Lymphocyte-induced Maturation Protein-1 (Blimp1).
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- The Innate Immune Memory That Bites Back: How Periodontitis May Train Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2026Review
- The osteoclast intracellular environment fosters bacterial growth duringbioRxiv : the preprint server for biology · 2026Article
- Lactobacillus sakei CVL-001 Inhibits Osteoclast Differentiation Through TLR2 and GPCR-Dependent Pathways and Prevents Bone Loss in Ovariectomized Mice.Probiotics and antimicrobial proteins · 2026Article
- Antiarthritic activities of berberine in a rat model of gouty arthritis.Scientific reports · 2025Article
- Osteomodulin modulates the inflammatory responses via the interleukin-1 receptor 1/nuclear factor-κB signaling pathway in dental pulpitis.International journal of oral science · 2025Article
- Integrating natural products with modern medicine in the treatment of gouty arthritis: a review.Inflammopharmacology · 2025Review
- Nanostructured lipid carriers in Rheumatoid Arthritis: treatment, advancements and applications.Inflammopharmacology · 2025Review
- Review
- Activation of liver X receptors suppresses the abundance and osteoclastogenic potential of osteoclast precursors and periodontal bone loss.Molecular oral microbiology · 2024Article
- Staphylococci planktonic and biofilm environments differentially affect osteoclast formation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Identification of molecular subgroups in osteomyelitis induced by staphylococcus aureus infection through gene expression profiles.BMC medical genomics · 2023Article
- MiRNA-23a-5p is the biomarkers for gouty arthritis and promotes inflammation in rats of gouty arthritis via MyD88/NF-κB pathway by induction TLR2.Archives of rheumatology · 2022Article
- Context-Dependent Roles for Toll-Like Receptors 2 and 9 in the Pathogenesis of Staphylococcus aureus Osteomyelitis.Infection and immunity · 2022Article
- Recent advances in enzyme-related biomaterials for arthritis treatment.Frontiers in chemistry · 2022Review
- Inhibitory Effects of Astaxanthin on CML-HSA-Induced Inflammatory and RANKL-Induced Osteoclastogenic Gene Expression in RAW 264.7 Cells.Biomedicines · 2021Article
- Ibudilast Mitigates Delayed Bone Healing Caused by Lipopolysaccharide by Altering Osteoblast and Osteoclast Activity.International journal of molecular sciences · 2021Article
- NF-κB responds to absolute differences in cytokine concentrations.Science signaling · 2021Article
- Macrophage-Osteoclast Associations: Origin, Polarization, and Subgroups.Frontiers in immunology · 2021Review
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Interleukin-20 Acts as a Promotor of Osteoclastogenesis and Orthodontic Tooth Movement.Stem cells international · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Toll-like receptors (TLR) and the receptor for interleukin-1 (IL-1R) signaling play an important role in bacteria-mediated bone loss diseases including periodontitis, rheumatoid arthritis, and osteomyelitis. Recent studies have shown that TLR ligands inhibit the receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation from un-committed osteoclast precursors, whereas IL-1 potentiates RANKL-induced osteoclast formation. However, IL-1R and TLR belong to the same IL-1R/TLR superfamily, and activate similar intracellular signaling pathways. Here, we investigate the molecular mechanisms underlying the distinct effects of IL-1 and Porphyromonas gingivalis lipopolysaccharide (LPS-PG) on RANKL-induced osteoclast formation. Our results show that LPS-PG and IL-1 differentially regulate RANKL-induced activation of osteoclast genes encoding Car2, Ctsk, MMP9, and TRAP, as well as expression of NFATc1, a master transcription factor of osteoclastogenesis. Regulation of osteoclast genes and NFATc1 by LPS-PG and IL-1 is dependent on MyD88, an important signaling adaptor for both TLR and IL-1R family members. Furthermore, LPS-PG and IL-1 differentially regulate RANKL-costimulatory receptor OSCAR (osteoclast-associated receptor) expression and Ca(2+) oscillations induced by RANKL. Moreover, LPS-PG completely abrogates RANKL-induced gene expression of B lymphocyte-induced maturation protein-1 (Blimp1), a global transcriptional repressor of anti-osteoclastogenic genes encoding Bcl6, IRF8, and MafB. However, IL-1 enhances RANKL-induced blimp1 gene expression but suppresses the gene expression of bcl6, irf8, and mafb. Our study reveals the involvement of multiple signaling molecules in the differential regulation of RANKL-induced osteoclastogenesis by TLR2 and IL-1 signaling. Understanding the signaling cross-talk among TLR, IL-1R, and RANK is critical for identifying therapeutic strategies to control bacteria-mediated bone loss.
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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.