We also show that amplification of PGE2 production by the simultaneous presence of bacteria and cytokines is fibroblast-specific, is mediated by the p38 mitogen-activated protein kinase (MAPK) pathway, and may drive excessive IL-8 production by macrophages, identifying a potential new mechanism responsible for the stromal-immune cross-talk in periodontitis. This evidence concerns the gene MAPK14 and periodontitis.