en پریودنتولوژی Periodontology پژوهشي Research <p> <strong>Background:</strong> Fibroblasts are now seen as active components of the immune response because these cells express Toll-like receptors (TLRs), recognize pathogen-associated molecular patterns, and mediate the production of cytokines and chemokines during inflammation. The innate host response to lipopolysaccharide (LPS) from Porphyromonas gingivalis is unusual inasmuch as different studies have reported that it can be an agonist for Toll-like receptor 2 (TLR2) and an antagonist or agonist for Toll-like receptor 4 (TLR4). This study investigates and compares whether signaling through TLR2 or TLR4 could affect the secretion of interleukin (IL)-6, IL-8, and stromal derived factor-1 (SDF-1/CXCL12) in both human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPDLF). </p><p> <strong>Methods:</strong> After small interfering RNA-mediated silencing of TLR2 and TLR4, HGF and HPDLF from the same donors were stimulated with P. gingivalis LPS or with two synthetic ligands of TLR2, Pam2CSK4 and Pam3CSK4, for 6 hours. IL-6, IL-8, and CXCL12 mRNA expression and protein secretion were evaluated by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. </p><p> <strong>Results:</strong> TLR2 mRNA expression was upregulated in HGF but not in HPDLF by all the stimuli applied. Knockdown of TLR2 decreased IL-6 and IL-8 in response to P. gingivalis LPS, or Pam2CSK4 and Pam3CSK4, in a similar manner in both fibroblasts subpopulations. Conversely, CXCL12 remained unchanged by TLR2 or TLR4 silencing. </p><p> <strong>Conclusion:</strong> These results suggest that signaling through TLR2 by gingival and periodontal ligament fibroblasts can control the secretion of IL-6 and IL-8, which contribute to periodontal pathogenesis, but do not interfere with CXCL12 levels, an important chemokine in the repair process. </p><hr><p></p><p> <strong>Source: </strong>Journal of Periodentology </p><p><a href="http://www.joponline.org/doi/abs/10.1902/jop.2012.120177" target="_blank"><font color="#0000ff"> Full Text</font></a></p> Cytokines, fibroblasts, gene silencing, Porphyromonas gingivalis, Toll-like receptor 2, Toll-like receptor 4 0 0 http://idai.ir/browse.php?a_code=A-10-32-1285&slc_lang=en&sid=1 Ana Carolina F. Morandini 10031947532846005666 10031947532846005666 No Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, São Paulo, Brazil Pedro Paulo Chaves Souza 10031947532846005667 10031947532846005667 No Department of Physiology and Pathology, Araraquara Dental School, São Paulo State University, Araraquara, São Paulo Erivan Schnaider Ramos-Junior 10031947532846005668 10031947532846005668 No Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, São Paulo Daniel Thomas Brozoski 10031947532846005669 10031947532846005669 No Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, São Paulo, Brazil Carla Renata Sipert 10031947532846005670 10031947532846005670 No Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, São Paulo, Brazil Carlos Alberto Souza Costa 10031947532846005671 10031947532846005671 No Department of Physiology and Pathology, Araraquara Dental School, São Paulo State University, Araraquara, São Paulo Carlos Ferreira Santos cebola@usp.br 10031947532846005672 10031947532846005672 Yes Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, São Paulo, Brazil