Abstract
Acute inflammatory response is uniform adaptive response of the body to breach its integrity initiated by humoral factors (cytokines, proinflammatory lipid mediators) and the hypothalamic-pituitary-adrenal axis. Under physiological state is effective defensive reaction that spontaneously subsides.
Magnitude of local acute inflammatory response and in its generalized form represents a systemic inflammatory response syndrome (SIRS). Starting proinflammatory processes is vital lifesaving responses, but overshooting of this reaction at the lack of anti-inflammatory mediators function has the same disastrous consequences as a failure proinflammatory response.
If the anti-inflammatory response is slowed down and braked in time, develop a critical catabolic state characterized by inflammatory mediators and cytokines storm with subsequent organ failure. Simultaneously with SIRS initiates file phenomena known as compensatory anti-inflammatory response syndrome (CARS), which represents a negative feedback system cytokine network, processes and endocrine activity mediators nonprotein - lipid mediators, among which include, besides the classical prostanoids also hepoxiliny, Protektin, resolviny and maresiny.
Creation of anti-inflammatory lipid mediators depends primarily on the availability of their precursors, in particular EPA and DHA, their conversion to target mediators, their transport and availability in the cell membranes. Currently also observed antiinflammatory role of lipid mediators in chronic subclinical inflammation accompanying metabolic diseases such as obesity, metabolic syndrome, diabetes mellitus, non-alcoholic steatohepatitis, and neurodegenerative diseases.
It is assumed that dysregulation antiinflammatory processes could significantly contribute to the initiation and maintenance of inflammation in chronic metabolic diseases.