Introduction

Mild cases of hidradenitis suppurativa (HS) are characterized as recurrent isolated nodules, while severe cases of the disease with chronic inflammation may lead to scarring, functional impairment, and squamous cell carcinoma. The disease arises most commonly in any skin bearing apocrine glands and it has recently become regarded as a disorder of the follicular epitheli um, with follicular occlusion giving rise to clinical findings. Follicular hyperkeratosis is the initial event, leading to occlusion followed by dilatation and follicular rupture, spilling contents, including keratin and bacteria, into the surrounding dermis with resultant secondary infection. These events induce a vigorous chemotactic response with an inflammatory cellular infiltrate consisting of neutrophils, lymphocytes, and histiocytes. Abscess formation develops leading to the destruction of the pilosebaceous unit. HS and acne vulgaris together with pilonidal sinus and dissecting cellulitis all share follicular occlusion as an initial event leading to disease development. Furthermore, bacterial colonization can increase the severity of chronic inflammation both in HS and acne vulgaris.

In healthy individuals as well as in mild cases of HS, the deeper layers of the skin remain free of infection, although it is constantly exposed to injuries and challenged by environmental microorganisms. This suggests that skin itself has the ability to fight against invading microbes. This chapter will summarize recent findings concerning the role of pattern recognition re ceptors (PRRs), antimicrobial peptides and proinflammatory cytokines/chemokines in innate and acquired immune responses of the skin.

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