The Mechanisms of the Regulation of Immune Response in Patients with Comorbidity of Chronic Obstructive Pulmonary Disease and Asthma

Background. Comorbidity of chronic obstructive pulmonary disease (COPD) and asthma (asthma COPD overlap syndrome, ACOS) is a significant problem in pulmonary practice, whose pathogenetic issues are not clarified yet. Objective. To study the features of the regulation of immune response in patients with comorbid COPD and asthma. Methods. We assessed the levels of CD3+, CD4+, CD8+, CD4+/CD8+, CD19+, CD25+, HLA-DR, total IgE, TNF-α, IL-4, IFN-γ, TXB2, and LTB4 in patients with comorbid COPD and asthma. Results. The study involved 44 people with COPD, 39 people with asthma, and 12 people with comorbid COPD and asthma. The specific features in comorbid COPD and asthma were lymphocytosis, increased absolute count of T-helper cells, increased cytotoxic T-lymphocytes in relative and absolute count, increased relative and absolute numbers of B-lymphocytes, and high levels of total IgE. The elevated levels of TNF-α and IL-4 and inhibition of IFN-γ production were detected. The content of LTB4 was maximal; TXB2 levels were higher than in control group but lower than in COPD and asthma. Conclusion. In comorbid COPD and asthma inflammation increased even during stable period. High levels of eicosanoids, low production of Th1-type cytokines, and active synthesis of opposition IL-4, along with increased IgE, indicate the activation of Th2-type immune response

Regulatory signal mechanisms of systemic inflammation in respiratory pathology

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