Start and finish of a physiological inflammatory reaction in wound healing and situations of microbial challenge. Cellular damage and leakage of alarmins attract neutrophils to the damaged area (PMN's). Sympathetic afferents activate the locus coeruleus (central nucleus of the sympathetic nervous system, SNS) and Noradrenaline (Norepinephrine, NE) is released. The released NE activates the adrenal medulla inducing the production of systemic catecholamins that supports the activation of the PMN. Damaged blood vessels are a source of an omega 3 rich edema (EPA and DHA). DHA and EPA inhibit LOX-5 directly and through conversion into resolvins and protectins. Both PGE2 and PGD2, produced by the breakdown of AA by COX-2 activity, will now override the strong chemotaxic effect of LTB4. The combined action of protectins, resolvins and lipoxins produced out of AA will put a hold on the pro-inflammatory activity of PMN's, which is supported by the increased production of systemic cortisol. Cortisol further activates macrophages (M-Ph) to phagocytose issue debris and quiet PMN by releasing substances such as LXA4, resolvin E1 (RvE1), prostanoid D1 (PD1), fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF) and epithelial growth factor (EGF) at the same time. Further edema leakage will be stopped, whereas angiogenesis and production of connective tissue will take place, finishing the inflammatory reaction and starting the production of new tissue.