ABSTRACT
Acne vulgaris is a disease of pilosebaceous units. Major hypotheses on its
pathophysiology include the following (1,2):
1. Altered follicular keratinization (hyperkeratinization) of the pilosebaceous
unit (3)
2. Propionibacterium acnes (P. acnes) follicular colonization and activity (4)
3. Hormonal influence (5-7)
4. Sebum production (8)
5. Release of inflammatory mediators (4,9)
These hypotheses have traditionally been viewed as independent factors
that, as a whole, contribute to acne pathogenesis. In particular, inflammation has
been viewed as a distinct contributor to acne, but the mechanism by which this
occurred was not well elucidated. Recent advances in molecular and cellular
studies now reveal that inflammation promotes acne via activation of the innate
immune system. In addition, studies now show that mechanisms involving the
innate immune system could initiate and influence many of the traditionally
described factors in acne pathogenesis, as listed above (1,10-12). The impor-
tance of the innate immune system in the pathogenesis of acne is a significant
advance in our understanding of acne with important implications for treatment.
Therefore, this chapter focuses on new and evolving insights into the role of the
innate immune system in association with acne, specifically on the manner in
which these new findings build upon traditionally known pathogenetic factors
and suggest additional hypotheses of acne pathophysiology. These new hypo-
theses include the following:
