Abstract

Interstitial pulmonary fibrosis is characterized by an abnormal accumulation of fibroblasts with a resultant increase in lung collagen content. Previous research has implied a possible involvement of the T-lymphocyte in this process. We used cyclosporin A (Cy A), a known immunosuppressant, to deplete T-lymphocyte-dependent responses in animals following treatment with agents known to produce fibrosis; butylated hydroxytoluene (BHT), bleomycin and beryllium (Be). BHT-treated mice and bleomycin-treated rats showed significant reduction in total lung hydroxyproline content with Cy A ( P < 0.05). These results suggest a contribution of the T-lymphocyte in the overall process of fibrosis, but do not indicate its role as the sole causative agent.

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