INTRODUCTION
Rosacea and acne vulgaris are common, chronic skin conditions that share an inflammatory pathogenesis, although their etiology is otherwise distinct. More recent research into the molecular and cellular pathophysiology
of these conditions indicates that antimicrobial peptides, part of the skin's immune response, play a key role in the inflammation seen in both of these skin disorders.1,2 Increased understanding of the mechanisms of this inflammation has brought
a new perspective on existing treatments for rosacea and acne. Here we review the role of inflammation in rosacea and acne, as well as the mechanisms by which commonly prescribed topical and oral medications reduce inflammation and treat these skin disorders.
Role of Inflammation in Disease Processes of Rosacea and Acne
Rosacea and Inflammation
Signs and symptoms of rosacea include papules and pustules, erythema and telangiectasia. Based on presenting symptoms, rosacea is further categorized as one of four subtypes: erythematous (subtype 1), with flushing, redness and telangiectasia;
papulopustular (subtype 2), characterized by papules and pustules, but also frequently featuring erythema and telangiectasia; phymatous (subtype 3), in which the skin thickens and enlarges, most commonly around the nose; or ocular (subtype 4). Most available treatments target papulopustular rosacea.3
The exact cause of rosacea is not known. For many patients, sun exposure, certain foods and other environmental factors can spark flares. The skin barrier is known to be impaired in patients with rosacea,4 resulting in increased transepidermal water loss,
which may contribute to feelings of dryness. A role has also been hypothesized for Demodex folliculorum, mites frequently found in the skin of patients with rosacea.5 Most recently, research has shown that antigens from a bacterium found in Demodex, Bacillus
oleronius, stimulate an inflammatory response in patients with papulopustular rosacea, but not in normal controls.6
Recent investigation into the inflammatory response of the skin suggests that in patients with rosacea, the natural immune response of the skin is dysregulated, resulting in chronic inflammation. Gallo and Yamasaki have observed that cathelicidins,
immune peptides in the skin that perform antimicrobial, chemotactic and angiogenic functions, are found at increased levels in patients with rosacea,1,7,8 likely due to increased levels of serine protease kallikrein 5 (KLK5), also known as stratum corneum
tryptic enzyme (SCTE), which upregulates cathelicidin expression.7 Levels of these same cathelicidin-producing enzymes are elevated in patients with milder forms of barrier disruptions, in which skin inflammation is not clinically apparent.9 At elevated
levels, like those seen in patients with rosacea, cathelicidins are likely to contribute to inflammation, attracting mast cells and other immune cells to the area and encouraging angiogenesis,1
