Medeiros, Marcell Costa de [UNESP]Tfaile Frasnelli, Sabrina Cruz [UNESP]Bastos, Alliny de Souza [UNESP]Orrico, Silvana Regina Perez [UNESP]Rossa Júnior, Carlos [UNESP]2014-12-032014-12-032014-05-01Journal Of Applied Oral Science. Bauru-sp: Univ Sao Paulo Fac Odontologia Bauru, v. 22, n. 3, p. 185-193, 2014.1678-7757http://hdl.handle.net/11449/112501Objective: The aim of this study was to evaluate a possible synergism between AGE-RAGE and TLR4 signaling and the role of p38 MAPK and NF-kB signaling pathways on the modulation of the expression of inflammatory cytokines and proliferation of cells from the innate and adaptive immune response. Material and Methods: T lymphocyte (JM) and monocyte (U937) cell lines were stimulated with LPS and AGE-BSA independently and associated, both in the presence and absence of p38 MAPK and NF-kB inhibitors. Proliferation was assessed by direct counting and viability was assessed by a biochemical assay of mitochondrial function. Cytokine gene expression for RAGE, CCL3, CCR5, IL-6 and TNF-alpha was studied by RT-PCR and RT-qPCR. Results: RAGE mRNA expression was detected in both cell lines. LPS and AGE-BSA did not influence cell proliferation and viability of either cell line up to 72 hours. LPS and LPS associated with AGE induced expression of IL-6 and TNF-alpha in monocytes and T cells, respectively. Conclusions: There is no synergistic effect between RAGE and TLR signaling on the expression of IL-6, TNF-alpha, RAGE, CCR5 and CCL3 by monocytes and lymphocytes. Activation of RAGE associated or not with TLR signaling also had no effect on cell proliferation and survival of these cell types.185-193engPeriodontal diseasesDiabetes mellitusInnate immunityAcquired immunityAdvanced glycosylation end productsArtigo10.1590/1678-775720130593S1678-77572014000300185WOS:000337907600008Acesso abertoS1678-77572014000300185.pdf7383391319292040