Abstract
P.acnes is the only microorganism that has been isolated from sarcoid lesions. Many P.acnes genomes have been detected in sarcoid lymph nodes using quantitative PCR and in sarcoid granulomas by in situ hybridization. These suggest an etiologic link between P.acnes and some cases of sarcoidosis. A recombinant trigger-factor protein from P.acnes causes a cellular immune response in some patients with sarcoidosis, but not in subjects without sarcoidosis. The P.acnes trigger-factor protein causes pulmonary granulomas in some 25-50% of mice sensitized with the protein and adjuvant. The results of animal experiments suggest that sensitization with P.acnes trigger-factor protein induces granulomas only in mice infected by P.acnes, whereas mice without granulomas may be free of P.acnes in their lungs. This pathogenesis has been confirmed by further experiments involving mice and rabbits, in which the eradication of P.acnes by antibiotics prevented granulomas in these experimental models. P.acnes can cause latent infection in peripheral lung tissue and the mediastinal lymph nodes and persist intracellularly in a cell-wall-deficient form. This dormant form of P.acnes can be activated endogenously under certain environmental conditions (hormones, stress, living habits, etc.) and proliferate in cells at the sites of latent infection. Granulomatous inflammation occurs in sarcoidosis patients with hypersensitivity to intracellular proliferation of the cell-wall-deficient bacteria, which can infect other cells or organs when spread via the lymphatic system or blood stream. The timely use of antibiotics may not only kill the bacteria proliferating at the sites of disease activity, but also prevent endogenous activation of P.acnes. If long term administration of antibiotics eradicates dormant forms of the bacteria persistent in organs, it may lead to complete remission of sarcoidosis.
