| Summary: | The paper presents data from literature and own studies of regulatory mechanisms of systemic inflammatory response in chronic obstructive pulmonary disease (COPD) and asthma. At the heart of the formation of a systemic inflammatory reaction is a complex of disturbances in the regulation of intra- and intercellular signaling. Etiopathogenesis of COPD and asthma differs, but immune disorders and regulatory mechanisms of systemic inflammation in the diseases have common characteristics. There are multi-type Th immune responses in both COPD and asthma, the nature of which depends on severity or control of the disease. Mixed phenotypes Th1/Th17 and Th2/Th17 appear and are followed by the formation of Th17 type of immune response associated with a worsening of the disease. General mechanisms of maintenance of systemic inflammation in the diseases have been found. These include hyperproduction of cytotoxic eicosanoids, decreased expression of CB2 receptors, the formation of mitochondrial dysfunction due to violations of the fatty acid composition of the organelle, increased synthesis of nitric oxide. The authors presented a new view on the role of immune, lipoxygenase, nitroxidergic, endocannabinoid signaling systems in the formation of systemic inflammation in chronic respiratory diseases.
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