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BioMed Research International
Volume 2013 (2013), Article ID 603046, 11 pages
Research Article

Deciphering the Intracellular Fate of Propionibacterium acnes in Macrophages

1Unit Molecular Microbial Pathogenesis, Pasteur Institute, 75724 Paris, France
2Department of Molecular Biology, Max Planck Institute for Infection Biology, 10117 Berlin, Germany
3Department of Biomedicine, Aarhus University, Wilhelm Meyers Allé 4, Bartholin Building, 8000 Aarhus C, Denmark
4Department of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21231, USA
5Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA

Received 6 February 2013; Revised 7 May 2013; Accepted 22 May 2013

Academic Editor: Yoshinobu Eishi

Copyright © 2013 Natalie Fischer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Propionibacterium acnes is a Gram-positive bacterium that colonizes various niches of the human body, particularly the sebaceous follicles of the skin. Over the last years a role of this common skin bacterium as an opportunistic pathogen has been explored. Persistence of P. acnes in host tissue has been associated with chronic inflammation and disease development, for example, in prostate pathologies. This study investigated the intracellular fate of P. acnes in macrophages after phagocytosis. In a mouse model of P. acnes-induced chronic prostatic inflammation, the bacterium could be detected in prostate-infiltrating macrophages at 2 weeks postinfection. Further studies performed in the human macrophage cell line THP-1 revealed intracellular survival and persistence of P. acnes but no intracellular replication or escape from the host cell. Confocal analyses of phagosome acidification and maturation were performed. Acidification of P. acnes-containing phagosomes was observed at 6 h postinfection but then lost again, indicative of cytosolic escape of P. acnes or intraphagosomal pH neutralization. No colocalization with the lysosomal markers LAMP1 and cathepsin D was observed, implying that the P. acnes-containing phagosome does not fuse with lysosomes. Our findings give first insights into the intracellular fate of P. acnes; its persistency is likely to be important for the development of P. acnes-associated inflammatory diseases.