Evidence for diversity within Propionibacterium acnes: a comparison of the T-cell stimulatory activity of isolates from inflammatory acne, endocarditis and the laboratory

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BackgroundPropionibacterium acnes is primarily associated with the pathogenesis of acne vulgaris but reports are increasing in number implicating P. acnes in other diseases such as abscess formation, meningitis and endocarditis. The pathogenicity of P. acnes is thought to be partly due to the interaction of the bacterium with the immune system. Historically, investigations have focused on humoral and cell-mediated immune responses to P. acnes antigens without attention to the possibility that different antigens may be expressed by different isolates.ObjectiveInvestigations were performed to determine whether there were differences between a laboratory strain of P. acnes (P-37) and fresh clinical isolates in their ability to stimulate naive and adult lymphocytes.Material and methodsThe fresh isolates were collected from a patient with inflammatory acne and a patient with P. acnes-induced prosthetic valve endocarditis. The lymphocyte transformation assay was used to detect responses to whole-cell suspensions of stationary phase P. acnes isolates during 7 days of incubation.ResultsThe acne isolate was significantly more stimulatory for cord blood mononuclear cells (CBMNCs) than the laboratory isolate (P. acnes P-37) at day 4 of incubation. There were no significant differences between the three strains at any other time points. However, the isolate cultivated from inflammatory acne was significantly more stimulatory for peripheral blood mononuclear cells (PBMNCs) from acne donors than the endocarditis isolate or the laboratory strain at most time points. There were no significant differences between the endocarditis strain and the laboratory strain.ConclusionIt can be hypothesized that in case of P. acnes-induced endocarditis lymphocyte stimulation is a disadvantage for the microorganism and therefore a lack of lymphocyte stimulation may be relevant to the pathogenesis of endocarditis.

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