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

Intercellular signaling networks with high complexity cause a spectrum of mechanisms achieving chronic obstructive pulmonary disease (COPD) that still question many uncertainties. 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. 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.

The evaluation of inflammatory, anti-inflammatory and regulatory factors contributing to the pathogenesis of COPD in airways.

Introduction: Chronic obstructive pulmonary disease (COPD) is a progressive chronic disease leading to obstructive lung airways and airflow limitations. The background of COPD is extensive cytopathology and histopathology orchestrated by mostly chronic inflammation with the local release of inflammatory, anti-inflammatory and regulatory mediators, as well as further remodeling and shaping of local architecture. Inflammatory mechanisms are provided by complex intercellular signalling networks and regulation of locally occurring immune responses.