It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
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.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 São Paulo State University (UNESP), School of Dentistry, Department of Physiology and Pathology, Araraquara, Brazil (GRID:grid.410543.7) (ISNI:0000 0001 2188 478X); Federal University of Goiás (UFG), School of Dentistry, Goiânia, Brazil (GRID:grid.411195.9) (ISNI:0000 0001 2192 5801)
2 Umeå University, Department of Molecular Periodontology, Umeå, Sweden (GRID:grid.12650.30) (ISNI:0000 0001 1034 3451)
3 São Paulo State University (UNESP), School of Dentistry, Department of Physiology and Pathology, Araraquara, Brazil (GRID:grid.410543.7) (ISNI:0000 0001 2188 478X)
4 Ribeirão Preto Medical School, University of São Paulo, Department of Biochemistry and Immunology, Ribeirão Preto, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)
5 Umeå University, Department of Molecular Periodontology, Umeå, Sweden (GRID:grid.12650.30) (ISNI:0000 0001 1034 3451); Sahlgrenska Academy at University of Gothenburg, Centre for Bone and Arthritis Research at Department of Internal Medicine and Clinical Nutrition, Institute for Medicine, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582)