JUN and infection: Microbial ligands binding to TLR activates intracellular signaling pathways, such as the mitogen-activated protein kinases (MAPK:p38) pathway, and activates nuclear factors such as kappa B (NF-kB) and c-jun, which regulate the production of inflammation-related mediators such as interleukine-8 (IL-8), interleukine-10 (IL-10), and tumor necrosis factor-alpha (TNF-α) [10] in order to control infection [11].