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.

MATERIAL AND METHODS

In this study, lung tissue specimens obtained from 33 COPD patients and 49 control patients were analysed. Tissue samples were examined by hematoxylin and eosin staining. Immunoreactive cells positive for interleukin (IL)-1α (IL-1α), IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, and tumour necrosis factor-α (TNF-α) were detected by an immunohistochemistry (IHC) method.

RESULTS

We evaluated overall higher numbers of IL-7, IL-8 and IL-10 (mostly from few (0/+) to almost abundance (++++)) and overall less numbers of IL-1α and IL-6 (mostly from no positive (0) to numerous to abundance (+++/++++)) immunoreactive cells in airway epithelium and connective tissue of COPD affected lung. Furthermore, we evaluated statistically significant (P < 0.05) higher numbers of immunoreactive cells located in control group airway epithelium for IL-4, IL-6, IL-7, IL-10, and IL-12 compared to mucosal and submucosal connective tissue. Moreover, in COPD group airway epithelium for IL-1α, IL-4, IL-6, IL-7, IL-8, and IL-10. We found no statistically significant difference between the numbers of IL-12 and TNF-α immunoreactive cells in airway epithelium and connective tissue of COPD affected lung. In comparison with the control group, we found statistically significant (P < 0.05) higher numbers of immunoreactive cells positive for all examined markers in COPD group.

CONCLUSIONS

Increased numbers of IL-1α, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, and TNF-α immunoreactive cells highlight the local significance of these markers in COPD pathogenesis. Moreover, the pattern with dominance of immunoreactive cells in COPD affected airway epithelium over connective tissue is highlighting the essentials of epithelium in inflammatory signalling.