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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Pedro P. C. Souza, Pernilla Lundberg, Inger Lundgren, Fernando A. C. Magalhães, Claudio M. Costa-Neto, Ulf H. Lerner

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 B1 and B2 receptor expression in human gingival fibroblasts and in mouse gingiva. Both P. gingivalis LPS and the synthetic TLR2 agonist Pam2CSK4 increased kinin receptor transcripts. Silencing of TLR2, but not of TLR4, inhibited the induction of kinin receptor transcripts by both P. gingivalis LPS and Pam2CSK4. Human gingival fibroblasts (HGF) exposed to Pam2CSK4 increased binding sites for bradykinin (BK, B2 receptor agonist) and des-Arg10-Lys-bradykinin (DALBK, B1 receptor agonist). Pre-treatment of HGF for 24 h with Pam2CSK4 resulted in increased PGE2 release in response to BK and DALBK. The increase of B1 and B2 receptor transcripts by P. gingivalis LPS was not blocked by IL-1β neutralizing antibody; TNF-α blocking antibody did not affect B1 receptor up-regulation, but partially blocked increase of B2 receptor mRNA. Injection of P. gingivalis LPS in mouse gingiva induced an increase of B1 and B2 receptor mRNA. These data show that activation of TLR2 in human gingival fibroblasts as well as in mouse gingival tissue leads to increase of B1 and B2 receptor mRNA and protein. More... »

PAGES

2973

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-018-37777-z

DOI

http://dx.doi.org/10.1038/s41598-018-37777-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112397110

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30814538


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47 schema:description 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<sub>1</sub> and B<sub>2</sub> receptor expression in human gingival fibroblasts and in mouse gingiva. Both P. gingivalis LPS and the synthetic TLR2 agonist Pam<sub>2</sub>CSK<sub>4</sub> 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<sub>2</sub>CSK<sub>4</sub>. Human gingival fibroblasts (HGF) exposed to Pam<sub>2</sub>CSK<sub>4</sub> increased binding sites for bradykinin (BK, B<sub>2</sub> receptor agonist) and des-Arg<sup>10</sup>-Lys-bradykinin (DALBK, B<sub>1</sub> receptor agonist). Pre-treatment of HGF for 24 h with Pam<sub>2</sub>CSK<sub>4</sub> resulted in increased PGE<sub>2</sub> release in response to BK and DALBK. The increase of B1 and B2 receptor transcripts by P. gingivalis LPS was not blocked by IL-1β neutralizing antibody; TNF-α blocking antibody did not affect B<sub>1</sub> receptor up-regulation, but partially blocked increase of B<sub>2</sub> receptor mRNA. Injection of P. gingivalis LPS in mouse gingiva induced an increase of B<sub>1</sub> and B<sub>2</sub> 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<sub>1</sub> and B<sub>2</sub> receptor mRNA and protein.
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