Alveolar macrophage is believed to be a primary target cell and major participant in the evolution of lung fibrosis after asbestos inhalation. Alveolar macrophage are known to release a variety of substance that induce tissue damage and stimulate inflammatory cells and fibroblast.

Macrophage also release a variety of metabolite of arachidonic acid. Of these, PGE(2) is known to suppress fibroblast proliferation. Asbestos may be a very effective stimulus for fibroblasts without triggering the relase of PGE(2).

To assess the fibrogenic properties of asbestos according to kind and dosage of asbestos and the ability of PGE(2) to suppress the proliferation of fibroblast, alveolar macrophages cultured with crocidolite, amosite and chrysotile in presence or absence of PGE(2)10(-5)M. At 24 hours after alveolar macrophage cultured with various stimuli, the released fibronectin and TNF-alpha was measured. Viability of alveolar macrophages was observed and growth promoting activity of macrphage supernatant to fibroblasts was quantified.

The results were as follows;

1. The viability of alveoair macrophages stimulated with asbestos fiber was markedly decreased compared with control group except chrysotile 10 microgram group. Crocidolite and amosite were more cytotoxic than chrysotile.

2. All of asbestos augmented fibronectin production in concentration dependent fashion.

3. There was a significant positive correlation between TNF-alpha production in supernatant and fiber concentration.

4. Supernatant from alveolar macrophages cultured with asbestos were inducible a significant increase in fibroblast proliferation.

5. Incubation of avieolar macrophages with asbestos in the presence of PGE(2) resulted in significant decrease of TNF-alpha production in supernant.

6. Supernatant from alveolar macrophages cultured with asbestos were inducible a: sig nificnat decrease in fibroblast proliferation when PGE(2) was added. The result of this study strongly suggested that crocidolite and amosite were more cytotoxic and fibrogenic and exogenous PGE(2) suppressed fibroblast proliferation following exposed to asbestos.