Propionibacterium acnes host cell tropism contributes to vimentin-mediated invasion and induction of inflammation.
|Title||Propionibacterium acnes host cell tropism contributes to vimentin-mediated invasion and induction of inflammation.|
|Publication Type||Journal Article|
|Year of Publication||2012|
|Authors||Mak, TN, Fischer, N, Laube, B, Brinkmann, V, Metruccio, MME, Sfanos, KS, Mollenkopf, H-J, Meyer, TF, Brüggemann, H|
|Date Published||2012 Nov|
|Keywords||Acne Vulgaris, Cell Line, Endocytosis, Epithelial Cells, Gene Expression Profiling, Gene Knockdown Techniques, Host-Pathogen Interactions, Humans, Inflammation, Male, Propionibacterium acnes, Prostatitis, Vimentin|
The contribution of the human microbiota to health and disease is poorly understood. Propionibacterium acnes is a prominent member of the skin microbiota, but is also associated with acne vulgaris. This bacterium has gained recent attention as a potential opportunistic pathogen at non-skin infection sites due to its association with chronic pathologies and its isolation from diseased prostates. We performed comparative global-transcriptional analyses for P. acnes infection of keratinocytes and prostate cells. P. acnes induced an acute, transient transcriptional inflammatory response in keratinocytes, whereas this response was delayed and sustained in prostate cells. We found that P. acnes invaded prostate epithelial cells, but not keratinocytes, and was detectable intracellularly 7 days post infection. Further characterization of the host cell response to infection revealed that vimentin was a key determinant for P. acnes invasion in prostate cells. siRNA-mediated knock-down of vimentin in prostate cellsattenuated bacterial invasion and the inflammatory response to infection. We conclude that host cell tropism, which may depend on the host protein vimentin, is relevant for P. acnes invasion and in part determines its sustained inflammatory capacity and persistence of infection.
|Alternate Journal||Cell Microbiol|