I plan to continue my studies of the expression of hypersensitivity in the lung using simple chemicals (2, 4, 6, trinitro-1- Chlorobenzene, TNCB; Dinitrofluorobenzene, DNFB). Haptens used in the study are similar to chemicals (trimelletic anhydride, TMA) described as industrial hazards of workers in the plastics industry. I am interested in studying the immunological mechanisms that may contribute to the pulmonary interstitial disease that develops in hapten immune animals. The results of these studies will have relevance for understanding mechanisms of pulmonary disease caused by industrial or environmental chemicals that react like haptens. The animals will be primed with hapten via the skin or the lung and a pulmonary response will be elicited by intratracheal inoculation of the immunizing chemical. The reactions will be assayed by histological examination of lung tissue sections and/or by differential analysis of cells from lung lavage. A lesion demonstrating fibrotic changes in (hamster) lungs was observed 15-21 days after challenge. Nonspecific mechanisms of the experimental (hapten- induced) lung disease will be determined by detecting pulmonary collagen deposition synthesis and degradation. An increase in lung elastin has been recorded. The kinetics of elastin deposition will be followed. Pulmonary immune responses will be studied in various lymphoid compartments of the lung and systemic immune system by quantitating specific T-lymphocytes in proliferation, performing delayed type hypersensitivity and cytotoxic cell assays as well as quantitating serum antibody and specific antibody forming cells (AFC). The relationship augmented natural killer cell activity to the pulmonary disease will be considered. The lung lesions as well as the accompanying immune responses to the agents will be studied. The results from these studies will give new insights into the immune mechanisms that participate in the etiology of pulmonary interstitial disease and perhaps provide a link between cellular immunity and pathological changes within the lung.
| Hu, H; Stein-Streilein, J (1993) Hapten-immune pulmonary interstitial fibrosis (HIPIF) in mice requires both CD4+ and CD8+ T lymphocytes. J Leukoc Biol 54:414-22 |
| Kimura, R; Hu, H; Stein-Streilein, J (1992) Delayed-type hypersensitivity responses regulate collagen deposition in the lung. Immunology 77:550-5 |
| Kimura, R; Hu, H; Stein-Streilein, J (1992) Immunological tolerance to hapten prevents subsequent induction of hapten-immune pulmonary interstitial fibrosis (HIPIF). Cell Immunol 145:351-8 |
