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,
* Division of Dermatology,
Department of Microbiology and Immunology, and
Molecular Biology Institute, University of California, Los Angeles, School of Medicine, Los Angeles, CA 90095;
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
¶ Department of Dermatology, Skin Research Center, General Infirmary, University of Leeds, Leeds, United Kingdom; and
|| Genentech, South San Francisco, CA 94080
One of the factors that contributes to the pathogenesis of acne is
Propionibacterium acnes; yet, the molecular mechanism by
which P. acnes induces inflammation is not known. Recent
studies have demonstrated that microbial agents trigger cytokine
responses via Toll-like receptors (TLRs). We investigated whether TLR2
mediates P. acnes-induced cytokine production in acne.
Transfection of TLR2 into a nonresponsive cell line was sufficient for
NF-
B activation in response to P. acnes. In addition,
peritoneal macrophages from wild-type, TLR6 knockout, and TLR1 knockout
mice, but not TLR2 knockout mice, produced IL-6 in response to
P. acnes. P. acnes also induced
activation of IL-12 p40 promoter activity via TLR2. Furthermore,
P. acnes induced IL-12 and IL-8 protein production by
primary human monocytes and this cytokine production was inhibited by
anti-TLR2 blocking Ab. Finally, in acne lesions, TLR2 was expressed
on the cell surface of macrophages surrounding pilosebaceous follicles.
These data suggest that P. acnes triggers inflammatory
cytokine responses in acne by activation of TLR2. As such, TLR2 may
provide a novel target for treatment of this common skin
disease.
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