Morphological characteristics of COPD-affected lung tissue in the ontogenesis perspective

Chronic obstructive pulmonary disease (COPD) is characterized by progressive narrowing of airways, development of chronic inflammation, and clinically observable shortness of breath. The morphopathogenesis of COPD is known to be determined by cell and tissue damage under the oxidative stress conditions, the formation of chronic inflammation, as well as changes in local tissue immunity, including antimicrobial protection. However, the perspective of the ontogenesis of these events has been poorly studied. The study aimed to determine and evaluate the morphological characteristics of COPD-affected lung tissue in the ontogenesis perspective. In this study, 40 COPD patients were evaluated. The lung tissue material was obtained during fibrobronchoscopy. Immunoreactive cells in bronchial tissue were detected by biotin-streptavidin immunohistochemistry method for the following markers of IL-1α, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, TNF-α, MMP-2, TIMP-2, TGF-β1, Hsp-70, hBD-2, hBD-3, and hBD-4. Stained structures were graded semiquantitatively. For statistical analysis of the data, nonparametric statistical methods were used. The COPD course of elderly COPD patients was mostly worse compared to younger COPD individuals. COPD patients with chronic bronchitis, epithelial metaplasia and granulation tissue findings were statistically significantly older. In all COPD patients, we found increased numbers of IL-6 but decreased numbers of IL-8 and IL-7-immunoreactive cells with ageing. In elderly COPD patients aged ≥ 75 years, the numbers of IL-1α, IL-4, MMP-2, IL-6, IL-10 immunoreactive cells increased, but the numbers of IL-8, IL-7, and TGF-β1 immunoreactive cells decreased with ageing. Overall, the findings of all studied factors were associated with the ageing process in COPD. In COPD, ageing is associated with worsening of the course of the disease, as well as the persistence of inflammatory cytokines and altered remodeling with otherwise typical COPD morphopathogenesis events.