Adoptive transfer of experimental hypersensitivity pneumonitis in the LEW rat.

The pathogenesis of immune-mediated pulmonary inflammation following inhalation of antigen in sensitized subjects may involve specific cellular or humoral mechanisms, or both. We used adoptive transfer to document cellular mechanisms in an established LEW rat model of acute hypersensitivity pneumonitis. The optimal protocol utilized sensitized spleen cells cultured for 72 h in the presence of antigen and concanavalin A before intraperitoneal injection of 20 x 10(6) cultured cells into sublethally irradiated recipients. Experimental and control rats were subjected 7 d later to twice daily aerosol challenge for 1 or 3 d and examined 12 h after the last challenge. Histopathology was evaluated in one lung, and the other was lavaged and cells evaluated by flow cytometry for T cell phenotypes (CD4, CD8, and RT6, CD45R subsets). Histopathology and cell numbers for most phenotypes were increased in experimental over controls, but proportions were unchanged. Similar results were obtained in animals evaluated at both 24 and 72 h after initial challenge. Results indicate cellular participation in an established LEW rat model of HP. Significant increases in numbers of T cell phenotypes suggest an important role in pathogenesis, but no single phenotype could be incriminated by disproportionate numbers.