Regulation disorders of pulmonary lipid metabolism in chronic obstructive pulmonary disease

Abstract

Chronic obstructive pulmonary disease (COPD) is one of the most socially significant respiratory diseases. The development and progression of COPD is mainly associated with smoking, which leads to chronic inflammation of the respiratory tract, including both cellular and humoral immunological processes. Contribution in immune defense of the lungs of ATP-transporters (ABC) is of great interest. Three lipid transporters ABCA1, ABCG1 and ABCA3 are expressed in lung cells. The first two contribute to reverse cholesterol transport, ABCA3 is involved in surfactant formation. Objective: study the expression of ABCA1, ABCG1 and ABCA3 genes in smoking and COPD. Methods: the analysis was carried out on previously studied data sets (gene sets) obtained from the expression of Omnibus (GEO) genes. Results: gene expression in alveolar macrophages in smokers (set GSE2125) showed a significant decrease of gene expression of ABCA1, ABCG1, apolipoprotein L1, L3, L4. Gene expression in airway epithelium in smokers (sets GSE4498, GSE3320, GSE11906), showed no significant changes of gene expression ABCA1, ABCA3, ABCG1, apolipoprotein L3 and L6. Gene expression in alveolar epithelial type II cells in patients with COPD showed a significant decrease in the expression of genes ABCA1, ABCA3, ABCG1, apolipoprotein L1, L3, L6, increased expression of TLR3, TLR4 compared with healthy individuals (set GSE29133). Conclusion: smoking disrupts the reverse transport of cholesterol in macrophages and alveolar epithelium, which probably serves as a mechanism of inflammation progression, reduces the expression of apolipoprotein L, whose function is not well known, but is considered to be involved in immune processes.