Growth and characterization of fibroblasts obtained from bronchoalveolar lavage of patients with scleroderma

We describe the detection and the growth of fibroblasts with human smooth muscle cell differentiation features from bronchoalveolar lavage (BAL) fluid of 53% of patients with scleroderma, but not from healthy controls. The binding of alpha-actin, vimentin and desmin antibodies by scleroderma lung fi...

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Bibliographic Details
Published inJournal of rheumatology Vol. 19; no. 11; p. 1716
Main Authors Ludwicka, A, Trojanowska, M, Smith, E A, Baumann, M, Strange, C, Korn, J H, Smith, T, Leroy, E C, Silver, R M
Format Journal Article
LanguageEnglish
Published Canada 01.11.1992
Subjects
Actins - immunology
Adult
Antibodies - analysis
Antibodies - metabolism
Blotting, Northern
Bronchoalveolar Lavage Fluid - pathology
Cell Differentiation
Cell Division
Cells, Cultured
Collagen - genetics
Collagen - metabolism
Cytoskeletal Proteins - immunology
Desmin - immunology
Female
Fibroblasts - metabolism
Fibroblasts - pathology
Fibronectins - genetics
Fibronectins - metabolism
Humans
Male
Middle Aged
Muscle, Smooth - chemistry
Phenotype
Prospective Studies
RNA, Messenger - analysis
RNA, Messenger - genetics
Scleroderma, Systemic - epidemiology
Scleroderma, Systemic - pathology
Vimentin - immunology
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Summary:We describe the detection and the growth of fibroblasts with human smooth muscle cell differentiation features from bronchoalveolar lavage (BAL) fluid of 53% of patients with scleroderma, but not from healthy controls. The binding of alpha-actin, vimentin and desmin antibodies by scleroderma lung fibroblasts exceeded that of normal adult lung fibroblasts, indicating that scleroderma lung fibroblasts express some markers of human smooth muscle cell differentiation (myofibroblasts), which may account for differences in biological behavior. A mesenchymal cell phenotype was documented by mRNA analysis, showing high expression of collagen type I and fibronectin in these cells. Fibronectin is also released in significantly higher amounts by scleroderma alveolar macrophages than by macrophages from healthy donors.
ISSN:0315-162X