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PubMed1993

[Cytokines and pulmonary fibroses].

Pulmonary fibrosis corresponds to an accumulation of collagens and other proteins of the extracellular matrix in the interstitium and alveoli. Biochemical and cellular mechanisms of pulmonary fibrogenesis remain poorly understood. The cells of the alveolitis (macrophages, lymphocytes and neutrophils) play a key role in producing the factors which regulate the proliferation, chemotactism and secretory activity of the fibroblasts. Amongst these factors the cytokines (interleukins, interferons and growth factors) play a definite but very complex role. Certain cytokines stimulate in vitro the attraction and activation of cells of the alveolitis, as well as the multiplication, migration and secretory activity of fibroblasts. The following cytokines are involved: tumour necrosis factor alpha: (TNF alpha), interleukin 1 (IL-1), interleukin 6 (IL-6) interleukin 8 (IL-8) transforming growth factor beta (TGF beta), platelet derived growth factor (PDGF), insulin like growth factor 1 (IGF-1), fibronectin, monocyte chemotactic protein 1: (MCP-1). Other cytokines, principally the interferons (of alpha, beta or gamma type: IFN alpha, IFN beta, IFN gamma) inhibit in vitro and in vivo the proliferation and the production of collagen by fibroblasts. During the course of human pulmonary fibrosis or in experimental situations, the majority of the cytokines mentioned above are produced in excess in the lung. Without doubt they play an important role in the pathogenesis of fibrosis, even if it is not yet very well known how they interact and contribute in vitro to the process of fibrogenesis. Certain cytokines potentially regulating in the fibrosis are yet to be identified. In the future the use of cytokines and of their inhibitors will perhaps provide new therapies in pulmonary fibrosis.

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PubMedDate not supplied

[Effect of peptides, isolated from the tracheal mucosa, on alveolar macrophages and the nature of the course of fibrosing alveolitis in the rat].

Rats with bleomycin-induced pulmonary fibrosis were treated with a complex of low-molecular weight peptides isolated from the tracheal mucosa (PTM). Cytological examinations of bronchoalveolar lavage fluid from the animals receiving PTM revealed increases in the number of alveolar macrophages (AM) as compared to that in saline-treated rats. The AM obtained from PTM-treated animals also showed an enhanced phagocytic activity, as well as increased superoxide anion production when stimulated with the opsonized zymosan. However, basal superoxide production after PTM administration was reduced to normal values. These PTM effects of the AM paralleled the reduction of pulmonary fibrotic changes and myocardial hypertrophy. The findings suggest that the AM functional activity is mediated by PTM.

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