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Activation of Toll-like receptor 2 induces B1 and B2 kinin receptors in human gingival fibroblasts and in mouse gingiva

Journal article
Authors P. P. C. Souza
P. Lundberg
I. Lundgren
F. A. C. Magalhaes
C. M. Costa-Neto
Ulf H Lerner
Published in Scientific Reports
Volume 9
ISSN 2045-2322
Publication year 2019
Published at Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Language en
Links dx.doi.org/10.1038/s41598-018-37777...
Keywords nf-kappa-b, active rheumatoid-arthritis, necrosis-factor-alpha, porphyromonas-gingivalis, bone-resorption, up-regulation, prostaglandin, biosynthesis, cutting edge, lipopolysaccharide, bradykinin
Subject categories Rheumatology and Autoimmunity

Abstract

The regulation of the kallikrein-kinin system is an important mechanism controlling vasodilation and promoting inflammation. We aimed to investigate the role of Toll-like receptor 2 (TLR2) in regulating kinin B-1 and B-2 receptor expression in human gingival fibroblasts and in mouse gingiva. Both P. gingivalis LPS and the synthetic TLR2 agonist Pam(2)CSK(4) increased kinin receptor transcripts. Silencing of TLR2, but not of TLR4, inhibited the induction of kinin receptor transcripts by both P. gingivalis LPS and Pam(2)CSK(4). Human gingival fibroblasts (HGF) exposed to Pam(2)CSK(4) increased binding sites for bradykinin (BK, B-2 receptor agonist) and des-Arg(10)-Lys-bradykinin (DALBK, B-1 receptor agonist). Pre-treatment of HGF for 24 h with Pam(2)CSK(4) resulted in increased PGE(2) release in response to BK and DALBK. The increase of B-1 and B-2 receptor transcripts by P. gingivalis LPS was not blocked by IL-1 beta neutralizing antibody; TNF-alpha blocking antibody did not affect B-1 receptor up-regulation, but partially blocked increase of B-2 receptor mRNA. Injection of P. gingivalis LPS in mouse gingiva induced an increase of B-1 and B-2 receptor mRNA. These data show that activation of TLR2 in human gingival fibroblasts as well as in mouse gingival tissue leads to increase of B-1 and B-2 receptor mRNA and protein.

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