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Sensitivity to bleomycin-induced pulmonary fibrosis was tested in various strains of mice. Among the strains examined, ICR, C57BL/10(H-2b), and C3H/He(H-2k) mice were highly sensitive to the induced pulmonary fibrosis; C57BL/6(H-2b), DBA/2(H-2d), A/J(H-2a), B6C3F1 and BDF1 mice were moderately sensitive, and CBA/JN(H-2k), BALB/c(H-2d), CDF1 and CBF1 mice were less sensitive. In congenic mice, which differ from each other only in the H-2 locus, C57BL/10(H-2b) was highly sensitive; B10·D2(H-2d) was moderately sensitive; and B10·BR(H-2k) and B10·A(H-2a) were less sensitive. Thus, the sensitivity differed depending on the haplotype of the H-2 genes. Furthermore, non-H-2 genes also seemed to be involved in the sensitivity to the pulmonary fibrosis. There was no correlation between the sensitivity to pulmonary fibrosis and enzyme activities such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in the lung tissues, but the levels of reducing agents such as ascorbic acid and tocopherol in the lungs were inversely correlated with the sensitivity to the pulmonary fibrosis, except in the case of BALB/c and its F1 mice.

Pulmonary fibrosis in mice induced by peplomycin (PEP) was suppressed by administration of anti-inflammatory agents such as prednisolone and D-penicillamine during or after the administration of PEP. Pulmonary fibrosis was also suppressed by administration of cyclophosphamide, an immunosuppressive antitumor agent before, during or after the administration of PEP. The pulmonary fibrosis in athymic nude mice induced by PEP was less than that in normal mice. The low response in the nude mice was enhanced by transfer of thymocytes to the same level as that in the normal mice. This suggests that the immune system, especially thymus-dependent immunity, is involved in the pulmonary fibrosis induced by PEP.