The role of Propionibacterium acnes (P. acnes) isolated from a high percentage of patients with sarcoidosis by Dr. Honnma, as a cause of sarcoidosis was examined. Interleukin-2 (IL-2) production and the responsiveness to IL-2 of alveolar lymphocytes stimulated by P. acnes were examined in vitro in a guinea pig model. The animals were divided into 4 groups, normal guinea pigs (group 1), guinea pigs intracutaneously presensitized with P. acnes and intratracheally challenged by saline (group 2), guinea pigs presensitized as above and intratracheally challenged with P. acnes (group 3), and guinea pigs presensitized as above and intratracheally challenged by P. acnes-pyridine extract residue (P. acnes-PER)(group 4). The production of IL-2 by alveolar lymphocytes stimulated by P. acnes-PER for 48 hours was determined using the method described by Gillis et al. The responsiveness of alveoloar lymphocytes to IL-2 was evaluated by 3H-TdR uptake in the presence and absence of P. acnes-PER. The amount of IL-2 produced by alveolar lymphocytes was 0.6±1.1, 0.7±1.1, 21.2±27.9 and 329.4±294.1 u/ml (M±SD), respectively, in groups 1, 2, 3 and 4. The value of IL-2 production in groups 3 and 4, the intratracheally challenged groups, was significantly higher htna that in groups 1 and 2, the control groups (p<0.02, p<0.01). By contrast, the IL-2 production of peripheral lymphocytes in groups 1, 2, 3 and 4 was 0, 7.4±10.3, 8.6±15.7 and 9.3±8.9 u/ml, respectively. The amount of IL-2 produced was about one-tenth thar of alveolar lymphocytes. In the intratracheally challenged groups, the responsiveness to IL-2 of alveolar lymphocytes in the presence and absence of P. acnes-PER was 12,514±12,766 and 6,611±7,066 for group 3, and 12,362±9,414 and 5,818±5,494 dpm, respectively, for group 4. The responsiveness to IL-2 of alveolar lymphoctyes in group 4 was signifincantly increased by stimulation with P. acnes-PER (p<0.05), but that in groups 1 and 2, control groups, was not different. Our findings indicate that P. acnes-PER stimulated IL-2 production from alveolar lymphocytes and induced a functionally active state of alveolar lymphocytes to IL-2 in this guinea pig model. In conclusion, the role of alveolar lymphocytes in an animal model stimulated by P. acnes appears to be consistent with that obtained on the sarcoidosis patients we previously reported.
experimental pulmonary granulomatosis