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Propionibacterium acnes and inflammation in acne; P. acnes has T‐cell mitogenic activity
Author(s) -
Jappe U.,
Ingham E.,
Henwood J.,
Holland K.T.
Publication year - 2002
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.2002.04602.x
Subject(s) - propionibacterium acnes , antigen , t cell receptor , biology , peripheral blood mononuclear cell , antibody , superantigen , microbiology and biotechnology , immunology , t cell , immune system , acne , in vitro , biochemistry , genetics
Background Circumstantial evidence suggests that Propionibacterium acnes has a role in the inflammation of acne. This could be effected by antigenic or superantigenic or mitogenic reactions. Objectives The purpose of this investigation was to determine whether P. acnes had only antigenic activity or additional superantigenic and mitogenic activity. Methods A lymphocyte transformation assay was used to detect responses to a mixture of eight P. acnes whole cell isolates, and their supernatant culture fluids. In order to determine the nature of T‐cell reactions to P. acnes cells a mouse–antihuman major histocompatibility complex class II monoclonal antibody was used in the lymphocyte transformation assay to inhibit the antigenic stimulation of lymphocytes. An analysis of the T‐cell receptor (TCR) variable region β (BV) repertoire was undertaken using flow cytometry of the unstimulated and stimulated cells. Results Peripheral blood mononuclear cells (PBMNC) from adults with no history of acne responded strongly to stationary growth phase cells of P. acnes , less strongly to cells in the exponential growth phase. No response was detected to supernatant culture fluids. PBMNC from five cord blood samples (CBMNC) responded maximally after 3 and 7 days of incubation with stationary growth phase cells of P. acnes . The reaction of CBMNC to P. acnes cells was not suppressed completely by the blocking antibody. The analysis of the TCRBV repertoire indicated that P. acnes induced no deletion or over‐representation of certain BV element‐bearing T cells. The TCRBV analysis was repeated after preincubation with the blocking antibody. Deletion of T cells bearing certain BV components occurred and there was no over‐representation of T cells carrying certain BV components. Conclusions Two mechanisms of lymphocyte activation by P. acnes cells are proposed, antigen and mitogen driven. These results are consistent with the histological evidence of inflammation in acne lesions.