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.
Background. The innate and adaptive immune systems in lungs are maintained not only by immune cells but also by non-immune tissue structures, locally providing wide intercellular communication networks and regulating the local tissue immune response. Aims. The aim of this study was to determine the appearance and distribution of inflammatory, anti-inflammatory and regulatory cytokines in relatively healthy lung tissue samples. Material and Methods. We evaluated lung tissue specimens obtained from 49 patients aged 9-95 years in relatively healthy study subjects. Tissue samples were examined by hematoxylin and eosin staining. Interleukin-1 (IL-1), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-7 (IL-7), and interleukin-10 (IL-10) were detected by an immunohistochemistry (IMH) method. The number of positive structures was counted semiquantitatively by microscopy. Non-parametric tests were used to analyse the data. Results. IL-1-positive cells were mostly found in the bronchial cartilage and alveolar epithelium. Immunoreactive lung macrophages were also found. The numbers of IL-4, IL-6, IL-7, and IL-10 containing cells were also found in the bronchial epithelium (in addition to those previously listed). The number of positive structures varied from occasional to moderate, but was graded higher in cartilage. Overall, fewer IL-1-positive cells and more IL-10-positive cells were found. Almost no positive structures for all examined cytokines were found in connective tissue and bronchial glands. Conclusions. Relatively healthy lung tissue exhibits anti-inflammatory response patterns. The cytokine distribution and appearance suggest persistent stimulation of cytokine expression in lung tissue and indicate the presence of local regulatory and modulating patterns. The pronounced cytokine distribution in bronchial cartilage suggests the involvement of a compensatory local immune response in the supporting tissue.
Lung tissue remodeling requires complex interactions of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), transforming growth factor (TGF) family and heat shock protein 70 (Hsp70). We evaluated the appearance and distribution of MMP-2, TIMP-2, TGF-β1 and Hsp70 in lung tissue using immunohistochemistry. Stained structures were graded semiquantitatively. Overall, more MMP-2, TIMP-2, TGF-β1 and Hsp70 were observed in bronchial cartilage, bronchial and alveola repithelium, and among alveolar macrophages. We evaluated mostly alveolar macrophages, bronchial epithelial cells and mucosal fibroblasts stained for TGF-β1, MMP-2 and TIMP-2. We also assessed strong or moderate correlations between numbers of cells containing TGF-β1, MMP-2, TIMP-2 in patients ≥ 60 years old. The presence of less TGF-β1 and more MMP-2, TIMP-2 and Hsp70 containing cells in all tissue groups indicated that local regulation was more dependent on MMP-2, TIMP-2 and Hsp70 distribution. Fewer TIMP-2, Hsp70 and TGF-β1 immunoreactive cells in younger individuals and increased expression of Hsp70 in elderly individuals demonstrated the influence of aging in lung remodeling. Findings of MMP-2, TIMP-2 and TGF-β1 immunoreactive cells in elderly individuals indicate lung remodeling due to aging.
Chronic obstructive pulmonary disease (COPD) is strongly associated with progressive airway limitation where the key mechanism is abnormal airway remodelling of bronchial mucosa maintained by complex crosstalk of tissue remodelling and regulatory factors. The aim of this study was to determine the appearance and local distribution of tissue remodelling factors in COPDaffected lung tissue and to compare the findings with the control group. In this study, lung tissue specimens were obtained from 27 patients with COPD and 49 control patients. Tissue samples were examined by routine hematoxylin and eosin staining. Remodelling and regulatory factors matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2), transforming growth factor-β1 (TGF-β1), as well as heat shock protein-70 (Hsp-70) were detected by immunohistochemistry in airway mucosa. The numbers of positive structures were evaluated semiquantitatively. Non-parametrical statistical analysis was performed. Overall COPD-affected lung tissue presented chronic inflammation and tissue remodelling in routine histological analysis. Compared to the control group, statistically significant (P<0.05) difference was calculated between COPD affected lung tissue and control group with overall more immunoreactive cells containing MMP-2, TIMP-2 and TGF-β1 and less Hsp-70 immunoreactive bronchial epithelial cells, subepithelial connective tissue fibroblasts, bronchial smooth muscle cells and secretory cells of bronchial glands with more pronounced findings of TGF-β1, however, less Papers on Anthropology XXVI/2, 2017, pp. 157-167 COPD AFFECTED LUNG TISSUE REMODELLING DUE TO THE LOCAL DISTRIBUTION OF MMP-2, TIMP-2, TGF-β1 AND HSP-70 158 | Z. Vitenberga, M. Pilmane, A. Babjoniševa key role of these remodelling factors in COPD pathogenesis. Decrease of Hsp-70 proves increased cell damage in COPD-affected airway mucosa.
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