Curbing Inflammation through Endogenous Pathways: Focus on Melanocortin Peptides

Figure 1

The inflammatory response. Stimuli such as tissue injury or microbial invasion trigger the release of chemical mediators (complement, cytokines, eicosanoids, and other autacoids) that activate the leukocyte recruitment (onset). Neutrophils are the first cell type to be recruited, and then peripheral blood monocytes also accumulate at the inflammatory site (acute phase). These monocytes will eventually differentiate into a more phagocytic phenotype helping to neutralize the injurious element and to clear the tissues off apoptotic neutrophils (resolution phase). This proresolving macrophage (and the involvement of stromal cells cannot be excluded here either) orchestrate resolution, by releasing and/or responding to proresolving mediators, some of which have been discussed in this review (see main text). Eventually, fully differentiated cells that have cleared the site by debris, dead cells, and bacteria will leave (via the lymphatic?) and the previously inflamed tissue or organ will regain its functionality, with return to homeostasis.