If you aren’t personally affected by the skin condition rosacea, you might not even know what it is. However, it affects over 45 million people worldwide, mostly fair-skinned people of European descent. At first, it is characterized by blotchy flushing on the face/neck regions, but eventually causes semi-permanent redness, dialation of blood vessels in the face, itchy eyes, burning sensations, and bumps (see below). Obviously, not pleasant.
The reason underlying this condition has only just recently been pinpointed by Richard Gallo’s group, published this week in Nature Medicine. In a nutshell, patients with rosacea have higher than normal levels of a peptide called cathelicidin as well as stratum corneum tryptic enzymes. Most of the cathelicidin that rosacea patients possess is abnormal, the result of incorrect processing steps, and fundamentally different in structure than what normal people have. The stratum corneum tryptic (SCT) enzymes are responsible for the abnormal post-translational processing.
Gallo’s group confirmed this theory by injecting mice with cathelicidin proteins plus SCT enzymes and increasing protease activity through a targeted deletion of the serine protease inhibitor Spink5. These mice exhibited abnormal processing of cathelicidin and rosacea-like symptoms. Interestingly, one of the most common treatments for rosacea is tetracycline, which inhibits cathelicidin processing and was first prescribed due to its antibacterial effects.