Normal human skin supports the growth of resident microbiota and it is colonized with a wide variety of resident microorganisms. In addition to normal flora, the skin is constantly challenged by pathogens, most of which do not cause clinical symptoms. Besides microbial adherence and virulence, environmental and local factors as well as host immunity are important components of cutaneous infections. In particular, skin becomes more susceptible to infections when the epidermal barrier function is damaged or when the keratinocyte-mediated innate immune functions are inhibited.
The pilosebaceous unit is an important site of skin infections such as acne vulgaris, folliculitis, furunculosis, and carbunculosis. A common pathogen associated with infections in the pilosebaceous unit is P. acnes. Although acne vulgaris is not an infectious disease, the role of P.
acnes in the pathogenesis of acne is well documented [37, 40]. Recent results describing the expression of TLRs in the pilosebaceous unit together with the increased amount of bacteria in acne vulgaris suggest that inflammation found in acne is at least partially mediated by the TLR signaling pathways (Fig. 13.3) [40, 54].
Gram-negative organisms such as P. aeruginosa, Pasteurella multocida, B. burgdorferi, Salmonella typhi, Bartonella sp., Klebsiella rhino-scleromatis and Vibrio vulnificus are not typical residents of the skin's microbiota but may cause cutaneous infections [10, 71]. However, their differential recognition through various TLRs expressed on keratinocytes and the expression of antimicrobial peptides highly effective against Gram-negative bacteria play important roles in the rarity of Gram-negative skin infections.
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