1. Academic Validation
  2. LOX-1 is involved in TLR2 induced RANKL regulation in peri-implantitis

LOX-1 is involved in TLR2 induced RANKL regulation in peri-implantitis

  • Int Immunopharmacol. 2019 Dec;77:105956. doi: 10.1016/j.intimp.2019.105956.
Qian Zhang 1 Jie Liu 2 Lei Ma 2 Na Bai 2 Huirong Xu 3
Affiliations

Affiliations

  • 1 Department of Prosthodontics, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China. Electronic address: dentistqianzhang@126.com.
  • 2 Department of Prosthodontics, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
  • 3 Department of Pathology, ZiBo Central Hospital, ZiBo, Shandong Province, China.
Abstract

Purpose: To explore whether receptor activator of nuclear factor kappa-B ligand (RANKL) is involved in the nosogenesis of peri-implantitis and to reveal the regulatory mechanism in Porphyromonas gingivalis induced RANKL production.

Methods: Therefore, we collected peri-implant crevicular fluid (PICF) and gingival tissues from healthy implants and peri-implantitis patients. The expression of RANKL in samples was tested by ELISA, Western blot and immunofluorescence staining. The production of RANKL in THP-1 macrophages stimulated with P. gingivalis was detected by qRT-PCR and Western blot. Then macrophages were pre-treated with neutralizing Antibodies of Toll-like Receptor 2 (TLR2) or lectin-type oxidized LDL receptor 1 (LOX-1) and inhibitors of TLR2, LOX-1 or ERK1/2 before P. gingivalis stimulation to evaluate the roles of TLR2, LOX-1 and ERK1/2 in RANKL production by qRT-PCR and Western blot.

Results: The protein level of RANKL was higher in PICF of peri-implantitis patients than healthy implants. We observed increased RANKL expression in P. gingivalis infected macrophages compared to controls. RANKL induced by P. gingivalis stimulation was mediated by TLR2 and ERK1/2 signaling pathway in THP-1 macrophages. LOX-1 is involved in TLR2 induced RANKL expression.

Conclusion: RANKL was involved in peri-implantitis, and regulated by TLR2, LOX-1 and ERK1/2 signaling against P. gingivalis Infection. As the novel inflammation pathway triggers, TLR2 and LOX-1 which mediate RANKL production seems to be potential drug targets of peri-implantitis.

Keywords

LOX-1; Porphyromonas gingivalis; RANKL; TLR2; peri-implantitis.

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