1. ^*Department of Dermatology and Allergology, University of Szeged, Szeged, Hungary
2. ^†Dermatological Research Group of the Hungarian Academy of Sciences and the University of Szeged, Szeged, Hungary
3. ^‡Institute of Clinical Microbiology, University of Szeged, Szeged, Hungary

Correspondence: István Nagy, PhD, Department of Dermatology and Allergology, University of Szeged, 6720 Szeged, Korányi fasor 6, Hungary. Email: nagyi@mail.derma.szote.u-szeged.hu

Received 15 July 2004; Revised 8 December 2004; Accepted 21 December 2004.

Abstract

Acne is a chronic inflammatory disease of the pilosebaceous follicle. One of the main pathogenetic factors in acne is the increased proliferation of Propionibacterium acnes (P. acnes) in the pilosebaceous unit. We investigated whether direct interaction of P. acnes with keratinocytes might be involved in the inflammation and ductal hypercornification in acne. The capacities of different P. acnes strains to activate the innate immune response and the growth of cultured keratinocytes were investigated. We have found that two clinical isolates of P. acnes significantly induced human -defensin-2 (hBD2) messenger RNA (mRNA) expression; in contrast a third clinical isolate and the reference strain (ATCC11828) had no effect on hBD2 mRNA expression. In contrast, all four strains significantly induced the interleukin-8 (IL-8) mRNA expression. The P. acnes-induced increase in hBD2 and IL-8 gene expression could be inhibited by anti-Toll-like receptor 2 (TLR2) and anti-TLR4 neutralizing antibodies, suggesting that P. acnes-induced secretion of soluble factors in keratinocytes are both TLR2 and TLR4 dependent. In addition, the clinical isolate P. acnes (889) was capable of inducing keratinocyte cell growth in vitro. Our findings suggest that P. acnes modulates the antimicrobial peptide and chemokine expression of keratinocytes and thereby contributes to the recruitment of inflammatory cells to the sites of infections.