Porphyromonas gingivalis Mfa1 Induces Chemokine and Cell Adhesion Molecules in Mouse Gingival Fibroblasts via Toll-Like Receptors.
Yuhei TakayanagiTakeshi KikuchiYoshiaki HasegawaYoshikazu NaikiHisashi GotoKousuke OkadaIichiro OkabeYosuke KamiyaYuki SuzukiNoritaka SawadaTeppei OkabeYuki SuzukiShun KondoTasuku OhnoJun-Ichiro HayashiAkio MitaniPublished in: Journal of clinical medicine (2020)
Porphyromonas gingivalis Mfa1 fimbriae are thought to act as adhesion factors and to direct periodontal tissue destruction but their immunomodulatory actions are poorly understood. Here, we investigated the effect of Mfa1 stimulation on the immune and metabolic mechanisms of gingival fibroblasts from periodontal connective tissue. We also determined the role of Toll-like receptor (TLR) 2 and TLR4 in Mfa1 recognition. Mfa1 increased the expression of genes encoding chemokine (C-X-C motif) ligand (CXCL) 1, CXCL3, intercellular adhesion molecule (ICAM) 1 and Selectin endothelium (E) in gingival fibroblasts, but did not have a significant effect on genes that regulate metabolism. Mfa1-stimulated up-regulation of genes was significantly suppressed in Tlr4 siRNA-transfected cells compared with that in control siRNA-transfected cells, which indicates that recognition by TLR4 is essential for immunomodulation by Mfa1. Additionally, suppression of Tlr2 expression partially attenuated the stimulatory effect of Mfa1. Overall, these results help explain the involvement of P. gingivalis Mfa1 fimbriae in the progression of periodontal disease.
Keyphrases
- toll like receptor
- inflammatory response
- nuclear factor
- cell adhesion
- immune response
- induced apoptosis
- poor prognosis
- genome wide
- cell cycle arrest
- nitric oxide
- cystic fibrosis
- cancer therapy
- extracellular matrix
- bioinformatics analysis
- pseudomonas aeruginosa
- binding protein
- transcription factor
- genome wide identification
- hyaluronic acid
- candida albicans
- oxidative stress
- signaling pathway
- staphylococcus aureus