Am. J. Respir. Crit. Care Med., Vol 151, No. 4, Apr 1995, 1205-1210.
Adoptive transfer of experimental hypersensitivity pneumonitis in the LEW rat
HB Richerson, JD Coon and D Lubaroff
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.
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.
