An Insight into COPD Morphopathogenesis: Chronic Inflammation, Remodeling, and Antimicrobial Defense

Abstract

Background and Objectives: Intercellular signaling networks with high complexity cause a spectrum of mechanisms achieving chronic obstructive pulmonary disease (COPD) that still question many uncertainties. Materials and Methods: Immunoreactive cells in bronchial tissue obtained from 40 COPD patients and 49 healthy control subjects 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, hBD−4. Results: Overall the highest numbers (from mostly moderate (++) to abundance (++++)) of IL-1α, IL-4, IL-7, IL-8, IL-10, IL-12, MMP-2, TIMP-2, TGF-β1 immunoreactive cells were marked increasingly in the blood vessel wall, connective tissue, and bronchial epithelium of COPD-affected lung, respectively. We found statistically significant (p < 0.05) higher numbers of immunoreactive cells positive for all of examined interleukins, TNF-α, MMP-2, TIMP-2, TGF-β1, hBD-2, and hBD-3 in the COPD-affected lung compared to the control group, but not for Hsp-70 and hBD-4. Conclusions: COPD-affected lung tissue exhibits mostly inflammatory response patterns of increased IL-1α, IL-4, IL-8, IL-12, and TNF-α, especially in the airway epithelium. Increased MMP-2 and TGF-β1, but decreased Hsp-70, proposes pronounced tissue damage and remodeling in COPD. High numbers of hBD-2 and hBD-3 immunoreactive cells may highlight antimicrobial activity in COPD within stable regulation of local immunity.