Cellular sensitivity to collagen in bleomycin-treated rats.
Previous reports have suggested that immune mechanisms are involved in the induction of certain types of pulmonary fibrosis. In this study endotracheal bleomycin was used to induce pulmonary fibrosis in rats, and they were then examined for cellular sensitivity to homologous interstitial collagens isolated from lung. Results indicate that rats treated with bleomycin develop transient cellular sensitivity to homologous collagen. Immunity appears to be selective to type I collagen with minimal response to type III collagen. The kinetics of the development of autoimmunity paralleled the transient increase in collagen synthesis in response to bleomycin treatment. This response was abolished upon prior treatment of the challenging antigen with purified bacterial collagenase, but was resistant to trypsin digestion. This finding confirms the true collagenous nature of the stimulating antigen and eliminates the possibility of a noncollagenous contaminant as the effective agent in the antigen preparation. The data suggest that cellular sensitivity to homologous collagen in response to bleomycin treatment may play a role in the overall fibrotic response.
D000818:Animals; D001761:Bleomycin / Q000494:pharmacology*; D003094:Collagen / Q000494:pharmacology*; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects; D007700:Kinetics; D008213:Lymphocyte Activation / Q000187:drug effects; D003012:Microbial Collagenase / Q000494:pharmacology; D011658:Pulmonary Fibrosis / Q000276:immunology; D051381:Rats; D013154:Spleen / Q000166:cytology / Q000276:immunology; D014357:Trypsin / Q000494:pharmacology
D001761:Bleomycin; D003094:Collagen; D014357:Trypsin; D003012:Microbial Collagenase