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ORIGINAL STUDY
Expression of CTGF and TNFa in alveolar macrophages of patients with idiopathic pulmonary fibrosis before and after treatment with azathioprine or interferon-γ-1b
1
3rd Pneumonology Department, Sismanoglio General District Hospita
2
Department of Pneumonology, University Hospital of Alexandroupolis and Medical School Democritus University of Thrace, Greece
3
Department of Pathology and Digital Image Analysis 417 NIMTS Hospital
4
Bronchoalveolar Lavage Laboratory, Sismanoglio General District Hospital
Corresponding author
Demosthenes Bouros
Pneumonology, Medical School Democritus, University of Thrace Director, Department of Pneumonology, University General Hospital 68100 Alexandroupolis, Greece
Pneumonology, Medical School Democritus, University of Thrace Director, Department of Pneumonology, University General Hospital 68100 Alexandroupolis, Greece
Pneumon 2011;24(2):149-156
KEYWORDS
idiopathic pulmonary fibrosis azathioprine interferon-γ-1b bronchoalveolar lavage CTGF TNFα alveolar macrophages
ABSTRACT
Background:
Idiopathic pulmonary fibrosis (IPF) is a fatal lung disorder the aetiology of which is unknown and for which there is no effective therapy. Connective tissue growth factor (CTGF) and tumour necrosis factor alpha (TNFα) have been reported to participate significantly in the pathogenesis of the disease. The role of alveolar macrophages in the expression of these cytokines remains unclear.
Material and Methods:
Samples of bronchoalveolar lavage fluid (BALF) derived from 20 newly diagnosed patients with IPF before and after 6 months of treatment with either interferon (IFN-γ-1b) and prednisolone (10 patients) or azathioprine (AZA) and prednisolone (10 patients) and from 10 normal subjects (control group) were used for the analysis of CTGF and TNFα protein expression in the alveolar macrophages. The effectiveness of the two drug regimes on the pulmonary function tests (FEV1, FVC, DLCO) and PaO2 and PaCO2 of the patients with IPF was investigated.
Results:
Decreased CTGF protein expression was detected in the patients with IPF compared with the control group (p=0.001). TNFα expression in IPF patients did not differ from that of the normal control subjects. Neither of the drug regimes affected the protein expression of these factorsor the pulmonary function parameters.
Conclusion:
These findings suggest that the alveolar macrophages are not the main source of CTGF and TNFα in IPF. Treatment with either AZA or IFN-γ-1b did not result in any significant change in the protein expression of these factors.
Idiopathic pulmonary fibrosis (IPF) is a fatal lung disorder the aetiology of which is unknown and for which there is no effective therapy. Connective tissue growth factor (CTGF) and tumour necrosis factor alpha (TNFα) have been reported to participate significantly in the pathogenesis of the disease. The role of alveolar macrophages in the expression of these cytokines remains unclear.
Material and Methods:
Samples of bronchoalveolar lavage fluid (BALF) derived from 20 newly diagnosed patients with IPF before and after 6 months of treatment with either interferon (IFN-γ-1b) and prednisolone (10 patients) or azathioprine (AZA) and prednisolone (10 patients) and from 10 normal subjects (control group) were used for the analysis of CTGF and TNFα protein expression in the alveolar macrophages. The effectiveness of the two drug regimes on the pulmonary function tests (FEV1, FVC, DLCO) and PaO2 and PaCO2 of the patients with IPF was investigated.
Results:
Decreased CTGF protein expression was detected in the patients with IPF compared with the control group (p=0.001). TNFα expression in IPF patients did not differ from that of the normal control subjects. Neither of the drug regimes affected the protein expression of these factorsor the pulmonary function parameters.
Conclusion:
These findings suggest that the alveolar macrophages are not the main source of CTGF and TNFα in IPF. Treatment with either AZA or IFN-γ-1b did not result in any significant change in the protein expression of these factors.
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