Expression of CTGF and TNFa in alveolar macrophages of patients with idiopathic pulmonary fibrosis before and after treatment with azathioprine or interferon-γ-1b

SUMMARY.Backgrou nd: Idiopathic pulmonary fibrosis (IPF) is a fatal lungdisorder the aetiology of which is unknown and for which there isno effective therapy. Connective tissue growth factor (CTGF) andtumour necrosis factor alpha (TNFα) have been reported to participatesignificantly in the pathogenesis of the disease. The role of alveolarmacrophages in the expression of these cytokines remains unclear.Materials and Methods: Samples of bronchoalveolar lavagefluid (BALF) derived from 20 newly diagnosed patients with IPF beforeand after 6 months of treatment with either interferon (IFN-γ-1b) andprednisolone (10 patients) or azathioprine (AZA) and prednisolone(10 patients) and from 10 normal subjects (control group) were usedfor the analysis of CTGF and TNFα protein expression in the alveolarmacrophages. The effectiveness of the two drug regimes on thepulmonary function tests (FEV1, FVC, DLCO) and PaO2 and PaCO2 ofthe patients with IPF was investigated. Results: Decreased CTGFprotein expression was detected in the patients with IPF comparedwith the control group (p=0.001). TNFα expression in IPF patientsdid not differ from that of the normal control subjects. Neither ofthe drug regimes affected the protein expression of these factorsorthe pulmonary function parameters. Co nclusion: These findingssuggest that the alveolar macrophages are not the main source ofCTGF and TNFα in IPF. Treatment with either AZA or IFN-γ-1b did notresult in any significant change in the protein expression of thesefactors. Pneumon 2011, 24(2):149-156.