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Cell and Tissue Research

, Volume 351, Issue 2, pp 325–337

First Online: 23 February 2012Received: 19 January 2012Accepted: 25 January 2012


The skin constitutes a formidable barrier against commensal and pathogenic bacteria, which permanently and transiently colonise the skin, respectively. Commensal and pathogenic species inhabiting skin both express proteases. Whereas proteases secreted by commensals contribute to homeostatic bacterial coexistence on skin, proteases from pathogenic bacteria are used as virulence factors, helping them colonise skin with breached integrity of the epithelial layer. From these initial sites of colonisation, pathogens can disseminate into deeper layers of skin, possibly leading to the spread of infection. Secreted bacterial proteases probably play an important role in this process and in the deterrence of innate defence mechanisms. For example, Staphylococcus aureus proteases are essential for changing the bacterial phenotype from adhesive to invasive by degrading adhesins on the bacterial cell surface. Secreted staphylococcal proteases mediate pathogen penetration by degrading collagen and elastin, essential components of connective tissue in the dermis. The activation of the contact system and kinin generation by Streptococcus pyogenes and S. aureus proteases contributes to an inflammatory reaction manifested by oedema, redness and pain. Kinin-enhanced vascular leakage might help bacteria escape into the circulation thereby causing possible systemic dissemination of the infection. The inflammatory reaction can also be fueled by the activation of protease-activated receptors on keratinocytes. Concomitantly, bacterial proteases are involved in degrading antimicrobial peptides, disarming the complement system and neutrophils and preventing the infiltration of the infected sites with immune cells by inactivation of chemoattractants. Together, this provides protection for colonising and-or invading pathogens from attack by antibacterial forces of the skin.

KeywordsProtease Skin Host defense This work was supported by grants from the Polish Ministry of Science and Higher Education N N301 050439 to J.K. and from the National Institutes of Health grant DE 09761, USA, National Science Center 2011-01-B-NZ6-00268, Kraków, Poland, the European Community FP7-HEALTH-2010-261460 -GumsandJoints- and the Foundation for Polish Science TEAM project DPS-424-329-10 to J.P. The Faculty of Biochemistry, Biophysics and Biotechnology of the Jagiellonian University is a beneficiary of structural funds from the European Union POIG.02.01.00-12-064-08.

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Autor: Joanna Koziel - Jan Potempa


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