The Effects of γ-Interferon on Hyperoxia Induced Lung Fibrosis in Neonatal Mice † 1977

In the mouse model of hyperoxia-induced lung injury, pulmonary fibrosis, as evidenced by increased collagen deposition, is a characteristic pathologic feature γ-Interferon (γ-INF) has been shown to inhibit the proliferation of adult human fibroblast (Chest 1992; 101:1326) and inducers ofγ-INF have been reported to reduce mortality, associated with hyperoxic lung damage (Lab Invest 1984;50;62). Based on these findings, we postulated that the protective effects of γ-INF in hyperoxic lung injury could, in part, be explained by its ability to inhibit collagen deposition. To test this hypothesis, adult mice were bred, and their offspring, randomized at two days of age to continuously receive 85% Oxygen (O₂) or room air (RA) for 30 days. Within each of these groups, one subset received 3 intraperitoneal injections of γ-INF (0.05ug/gm) 3 times per, week. At 30 days, the lungs were prepared for histological examination and determination of collagen content (COL) and hydroxyproline (OHPR) content. Data are expressed as [mean(SD)]. Table

Table 1 No caption available.

γ-INF did not affect the reduction in final body weight in the animals exposed to O₂, however, γ-INF treatment significantly reduced the collagen and OHPR content (indices of pulmonary fibrosis) in the O2 exposed group. These findings indicate that γ-INF inhibits collagen formation in this model, and may be responsible for the reported protective action of the drug.