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CD209⁺ Macrophages Mediate Host Defense against Propionibacterium acnes¹

Philip T. Liu^2,*, Jenny Phan^2,*, Dominic Tang^*, Melissa Kanchanapoomi^*, Brian Hall, Stephan R. Krutzik^* and Jenny Kim^3,*

^* Division of Dermatology, Department of Medicine, David Geffen School of Medicine at University of California-Los Angeles, CA 90095; and Amnis Corporation, Seattle, WA 98121

Propionibacterium acnes is a major etiological factor of acne, triggering an inflammatory response in part through the activation of TLR2. In this study, we demonstrate that activation of peripheral blood monocytes with P. acnes in vitro induced their differentiation into two distinct innate immune cell subsets, CD209⁺ macrophages and CD1b⁺ dendritic cells. Furthermore, P. acnes induced expression of mRNA for the cytokines IL-15 and GM-CSF, which differentiate CD209⁺ and CD1b⁺ cells, respectively. The CD209⁺ cells were more effective in uptake of P. acnes, compared with the CD1b⁺ cells, and demonstrated a 2-fold greater antimicrobial activity against the phagocytosed bacteria. Although CD1b⁺ cells secreted inflammatory cytokines in response to both P. acnes and a TLR2 ligand control, the CD209⁺ cells responded only to P. acnes. The addition of all-trans retinoic acid, a commonly used agent for the treatment of acne, directly induced differentiation of monocytes into CD209⁺ macrophages and enhanced the P. acnes-mediated differentiation of the CD209⁺ subset. Therefore, the differentiation of monocytes into CD209⁺ macrophages and CD1b⁺ dendritic cells distinctly mediate the innate immune response to P. acnes.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by National Institutes of Health Grant K08 AR48551 and R01 AI059091. P.T.L. is supported by the Microbial Pathogenesis Training Grant 2-T32-AI-07323.

² P.T.L. and J.P. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Jenny Kim, Division of Dermatology, University of California-Los Angeles, 52-121 Center for Health Sciences 10833 Le Conte Avenue, Los Angeles, CA 90095. E-mail address: jekim{at}mednet.ucla.edu

⁴ Abbreviations used in this paper: ATRA, all-trans retinoic acid; CTC, 5-cyano-2,3-ditolyl tetrazolium chloride; MOI, multiplicity of infection; L, ligand.