Pulmonary histologic abnormalities resolve despite continuing intratracheal injections of Micropolyspora faeni in a rabbit model of hypersensitivity pneumonitis. We examined in vitro alveolar macrophage (AM) metabolism to determine if increased efficiency of M. faeni degradation by AMs was associated with resolution of pulmonary abnormalities. Rabbits were exposed to M. faeni with three sensitizing and two, four, or eight weekly intratracheal challenge injections. Bronchoalveolar cells (BAC) were obtained by lavage 4 to 6 days after the last intratracheal injection. We determined the fate of 125I-labeled M. faeni added to 48-hour cultures of BAC derived from naive and M. faeni-exposed animals. Label was transported from the pellet to the supernatant fraction of BAC cultures, and the proportion of supernatant label that was precipitated by trichloroacetic acid decreased. These phenomena were dependent on time, viable cells, and temperature. They were not altered by puromycin and were caused by AM. BAC from M. faeni-treated rabbits were slightly more effective in transport of label from pellet to supernatant than BAC from naive rabbits during the first 4 hours of culture but not thereafter. There was no difference between BAC from rabbits challenged two, four and eight times. We conclude that resolution of pulmonary histologic abnormalities in this model of hypersensitivity pneumonitis is not associated with evidence of enhanced AM particulate M. faeni catabolism.