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Platelet-derived growth factor-beta mRNA in human alveolar macrophages in vivo in asthma
I K Taylor1, M Sorooshian, A Wangoo
1Dept of Respiratory Medicine, St. Marys Hospital Medical School, London, UK.
Abstract:
Collagen deposition and myofibroblast proliferation beneath the epithelial basement membrane in patients with asthma is now increasingly recognized, although the molecular pathogenesis remains obscure. We have evaluated messenger ribonucleic acid (mRNA) expression of the profibrotic cytokine, platelet-derived growth factor-beta (PDGF-beta), in alveolar macrophages obtained following fibreoptic bronchoscopy and bronchoalveolar lavage in patients with asthma. Three subject groups were studied: 1) asthmatics using regular inhaled glucocorticoid medication (ASTST, n = 9), 2) asthmatics using intermittent inhaled beta 2-agonist therapy only (ASTBR, n = 10); 3) nonasthmatic control volunteers (n = 10). Alveolar macrophage mRNA was extracted and PDGF-beta mRNA quantified by reverse-transcriptase polymerase chain reaction (PCR) (RT-PCR) and expressed as the ratio to that of a control gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH). There were no significant differences in PDGF-beta mRNA expression between the groups, or between all asthmatic (n = 19) and control subjects. Furthermore, there was no correlation between alveolar macrophage PDGF-beta mRNA expression and airway spirometry, or duration of glucocorticoid usage or dose. Thus, in contrast to other fibrotic lung diseases, we found little evidence of enhanced expression of PDGF-beta mRNA in alveolar macrophages in clinically stable bronchial asthma.
Insights
This study found no significant difference in platelet-derived growth factor-beta messenger ribonucleic acid (mRNA) expression in alveolar macrophages of asthma patients compared to controls. This suggests PDGF-beta mRNA is not a key factor in stable asthma-related lung tissue changes.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Immunology
Background:
- Asthma pathogenesis involves collagen deposition and myofibroblast proliferation, but underlying molecular mechanisms are unclear.
- Platelet-derived growth factor-beta (PDGF-beta) is a profibrotic cytokine implicated in fibrotic lung diseases.
Purpose of the Study:
- To investigate the messenger ribonucleic acid (mRNA) expression of PDGF-beta in alveolar macrophages of asthma patients.
- To determine if PDGF-beta mRNA levels correlate with asthma severity or medication use.
Main Methods:
- Alveolar macrophages were collected from asthma patients (on glucocorticoids or beta 2-agonists) and non-asthmatic controls via bronchoscopy and bronchoalveolar lavage.
- PDGF-beta mRNA expression was quantified using reverse-transcriptase polymerase chain reaction (RT-PCR) and normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA.
- Statistical analysis compared PDGF-beta mRNA levels between groups and correlated them with spirometry and medication data.
Main Results:
- No significant differences in PDGF-beta mRNA expression were observed between asthma patient groups and controls.
- PDGF-beta mRNA levels did not correlate with airway spirometry, duration, or dose of glucocorticoid medication.
- Overall, asthmatic subjects showed no enhanced PDGF-beta mRNA expression in alveolar macrophages compared to controls.
Conclusions:
- In clinically stable asthma, enhanced PDGF-beta mRNA expression in alveolar macrophages is not evident.
- Unlike other fibrotic lung diseases, PDGF-beta may play a limited role in the molecular pathogenesis of stable asthma.
- Further research is needed to elucidate the specific molecular pathways driving fibrotic changes in asthma.