Normal human skin supports the growth of commensal microflora and it is colonized with a wide variety of microorganisms such as Propionibacterium acnes (P. Acnes), Staphylococcus epidermidis, and Malassezia furfur. In addition to normal flora, the skin is constantly challenged by a large number of external pathogens, most of which do not cause clinical symptoms. Importantly, in healthy individuals, the deeper layers of the skin remain free of infections suggesting that skin has the ability to fight against invading microbes . Indeed, skin has a powerful innate immune system that protects the host from bacterial and fungal infections. Within the epidermis, keratinocytes and sebocytes represent two, immunologically active cell types, which are able to identify and kill invading microbes. Keratinocytes and sebocytes recognize highly conserved structures of the pathogens, termed Pathogen-Associated Molecular Patterns (PAMPs), by Pattern Recognition Receptors (PRRs), such as Toll-like Receptors (TLRs). Signaling through PRRs activates a chemical cutaneous defense system which results in the production of pro-inflammatory cytokines/chemokines and antimicrobial peptides. Within the skin, these mediators possess dual function: they not only display direct microbicidal activity but also attract professional immune cells. Therefore, pro-inflammatory mediators play crucial role in a number of skin infections, forming complicated networks between keratinocytes, sebocytes, and infiltrates of immune cells. This crosstalk occurs, partly, via antimicrobial peptides and their receptors.
|Title of host publication||Pathogenesis and Treatment of Acne and Rosacea|
|Publisher||Springer-Verlag Berlin Heidelberg|
|Number of pages||8|
|ISBN (Print)||3540693742, 9783540693741|
|Publication status||Published - Nov 1 2014|
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