Abstract
Sarcoidosis is a systemic granulomatous disease of unknown etiology. Propionibacterium acnes is the only microorganism that has been isolated from sarcoid lesions. Many P. acnes have been detected in sarcoid lymph nodes using quantitative PCR and in sarcoid granulomas by in situ hybridization. P. acnes trigger factor protein causes a cellular immune response only in sarcoid patients and induces pulmonary granulomas in mice sensitized with the protein and adjuvant, but only those with latent P. acnes infection in their lungs. Eradication of P. acnes by antibiotics prevents the development of granulomas in this experimental model. Although P. acnes is the most common commensal bacterium in the lungs and lymph nodes, P. acnes-specific antibody detected the bacterium within sarcoid granulomas of these organs. P. acnes can cause latent infection in the lung and lymph node and persist in a cell-wall-deficient form. The dormant form is activated endogenously under certain conditions and proliferates at the site of latent infection. In patients with P. acnes hypersensitivity, granulomatous inflammation is triggered by intracellular proliferation of the bacterium. Proliferating bacteria may escape granulomatous isolation, spreading to other organs. Latent P. acnes infection in systemic organs can be reactivated by another triggering event, leading to systemic sarcoidosis.
Highlights
Sarcoidosis is one of the best-known systemic granulomatous diseases
We propose mechanisms of granuloma formation in response to this indigenous bacterium in subjects with sarcoidosis based on our results obtained using histopathological and experimental approaches and introduce a new concept of endogenous infection caused by hypersensitivity to indigenous bacteria
Ishige et al used quantitative polymerase chain reaction (PCR) to search for bacterial genomes of P. acnes, P. granulosum, and M. tuberculosis in histologic sections of lymph nodes from patients with sarcoidosis, tuberculosis, or gastric cancer [27]
Summary
Sarcoidosis is one of the best-known systemic granulomatous diseases. Despite intensive investigation, the etiology of sarcoidosis has remained unresolved for more than 100 years [1]. Sarcoidosis seems to result from the exposure of a genetically susceptible subject to an environmental agent, and microbial etiologies of sarcoidosis have long been considered based on the clinical similarities to infectious granulomatous diseases [2]. Immune responses are frequently detected in sarcoid patients as well as in some nonsarcoid patients and healthy subjects Latent infection by these organisms complicates the interpretation of the results of these immunologic studies. We propose mechanisms of granuloma formation in response to this indigenous bacterium in subjects with sarcoidosis based on our results obtained using histopathological and experimental approaches and introduce a new concept of endogenous infection caused by hypersensitivity to indigenous bacteria
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