The major effects of prostanoid lipid mediators are mediated through specific G-protein-coupled cell membrane receptors that differ in their expression and intracellular signaling pathways [ 46].
Although the major effects of COX-derived lipid mediators are mediated through cell surface receptors, some prostanoids and their metabolites may act on target cells through nuclear receptors located at the nuclear envelope [ 50].
The analgesic effect of nitrous oxide is mediated by endogenous mediators, including opioids in nature [ 22].
Whether the effect is mediated through specific mediators or non-inflammatory cells such as enteric nerves remains to be determined.
The restricted GLP2 receptor distribution has led to the proposal that the multitude of GLP2-induced effects is mediated by indirect mediators and diverse signaling pathways [ 40].
Stimulation of TLR5 by flagellin is mediated through the signaling mediators MAPK p38 and ERK, which also were elevated in the monocytes of older compared with younger donors.
Thus, depending on the phase of activation, IL-1 β and IL-6 could be considered as mediators of resolution of inflammation that is mediated through monocytes [9].
The adaptive immune response in AIA is dependent on antigen-specific CD4+ T cells and their derived mediators and, to a lesser extent, is mediated by serum antibodies [ 44, 45].
IGF-I signalling is mediated by a network of intracellular mediators that include the phosphatidylinositol-3-kinase/Akt pathway and the mitogen-activated kinase cascades.
Sepsis is mediated by many biologically active inflammatory mediators, including interleukins.
