Modulation of cell proliferation,survival and gene expression by RAGE and TLR signaling in cells of the innate and adaptive immune response: Role of p38 MAPK and NF-KB

Objective: the aim of this study was to evaluate a possible synergism between agerage 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-a 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-a in monocytes and t cells,respectively. conclusions: there is no synergistic effect between rage and tlr signaling on the expression of il-6,tnf-a,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.