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BALF-derived fibroblasts differ from biopsy-derived fibroblasts in systemic sclerosis

¹ Dept of Rheumatology, ³ Dept of Respiratory Medicine and Allergology, Lund University Hospital, ² Dept of Experimental Medical Science, Lund University, Lund, Sweden. ⁴ Dept of Radiology, London Chest Hospital, London, UK.

CORRESPONDENCE: A. Scheja, Dept of Rheumatology, Lund University Hospital, S-221 85 Lund, Sweden. Fax: 46 46128468. E-mail: Agneta.Scheja{at}med.lu.se

Keywords: Eosinophils, fibroblasts, granulocyte-macrophage colony-stimulating factor, pulmonary fibrosis, scleroderma, systemic sclerosis

Received: November 16, 2005
Accepted November 4, 2006

Growth of fibroblasts from bronchoalveolar lavage fluid (BALF) in patients with systemic sclerosis (SSc) has previously been described. The purpose of the present study was to characterise fibroblasts from BALF and bronchial biopsies from SSc patients with alveolitis and from controls, to analyse fibroblast proliferation, migration, stress fibres and proteoglycan production.

BALF and bronchial biopsies were collected from 10 patients with SSc and alveolitis and from 15 controls.

Outgrowth of fibroblasts was observed from the BALF of four patients, particularly in those with a markedly increased percentage of eosinophils in BALF, but not in any member of the control group. Increased levels of granulocyte-macrophage colony-stimulating factor, correlating with the percentage of eosinophils in BALF, were found in patients when compared with controls. Fibroblasts from BALF showed an elongated, mobile phenotype and increased proteoglycan production compared to the corresponding biopsy fibroblasts.

In conclusion, outgrowth of fibroblasts with an altered phenotype is reported from bronchoalveolar lavage fluid in systemic sclerosis patients with alveolitis and an increased percentage of eosinophils in the bronchoalveolar lavage fluid. These findings indicate a possible role for eosinophil–fibroblast interaction in pulmonary fibrosis in systemic sclerosis.

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