Higher TGF-β with lower CD124 and TSLP, but no difference in PAR-2 expression in bronchial biopsy of bronchial asthma patients in comparison with COPD patients
Language English Country United States Media print
Document type Clinical Trial, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Biopsy MeSH
- Asthma * metabolism pathology MeSH
- Bronchi metabolism pathology MeSH
- Pulmonary Disease, Chronic Obstructive * metabolism pathology MeSH
- Cytokines biosynthesis MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Interleukin-4 Receptor alpha Subunit biosynthesis MeSH
- Receptor, PAR-2 biosynthesis MeSH
- Gene Expression Regulation, Neoplastic * MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Thymic Stromal Lymphopoietin MeSH
- Transforming Growth Factor beta biosynthesis MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Clinical Trial MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- Cytokines MeSH
- IL4R protein, human MeSH Browser
- Interleukin-4 Receptor alpha Subunit MeSH
- Receptor, PAR-2 MeSH
- Thymic Stromal Lymphopoietin MeSH
- Transforming Growth Factor beta MeSH
Chronic obstructive pulmonary disease (COPD) and bronchial asthma (BA) are 2 severe respiratory disorders with different predominated immunopathologies. There are several "novel molecules" from different families that are proposed as part of the etiopathogenesis of COPD and BA. Proteinase-activated receptor 2 (PAR-2), thymic stromal lymphoprotein (TSLP), interleukin-4 and its receptor (CD124), Yin-Yang 1 (YY1), and transforming growth factor beta (TGF-β) have been previously shown to be involved in the pathophysiology of both these diseases. We investigated PAR-2, TSLP, CD124 (interleukin-4R), TGF-β, and YY1 immunohistochemical expression in endobronchial and transbronchial biopsies from 22 BA patients and 20 COPD patients. Immunostaining for the above-mentioned antigens was quantified using a modified semiquantitative scoring system and statistically evaluated. The values of TGF-β in the epithelial cells (P=0.0007) and TGF-β in the submucosa (P=0.0075) were higher in the BA samples, whereas values of CD124 (P=0.0015) and TSLP (P=0.0106) were higher in the COPD samples. No statistically significant differences between the groups were recorded for PAR-2 and YY1. Airway inflammatory reaction diversity in BA and COPD seems to be disease specific; however, there are also shared mechanisms involved in the pathophysiology of both diseases.
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