Parasites and inflammation fuel rosacea
Increasing evidence suggests that demodex mites may play a role in the pathogenesis of rosacea, a common, chronic inflammatory skin condition, according to the medical director of the Skin Centre for Dermatology in Peterborough, Ontario, Canada.
Speaking here to fellow Canadian dermatologists at Dermatology Update (Ontario, 2015), Melinda Gooderham M.D., M.Sc., F.R.C.P.C., discussed how demodex mites are in greater abundance on the skin of patients with rosacea compared to individuals without rosacea.
"If not demodex, what causes rosacea?" Dr. Gooderham says. "What are the triggers that are causing this inflammatory cascade?"
Dr. Gooderham explains that, in an intact innate immune system, activation of the toll-like receptors incites a cleavage of pro-cathelicidin into cathelicidin, noting cathelicidin possesses properties needed for an effective immune system.
All individuals have demodex mites on their face, Dr. Gooderham notes, but a dysregulated immune response is believed to lead to rosacea.
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It was observed in research that patients with rosacea have elevated expression of toll-like receptor 2 (TLR2) compared to patients with normal skin. Moreover, overexpression of TLR2 on keratinocytes, treatment with ligands of TLR2, and analysis of mice deficient in TLR2 led to a calcium-dependent discharge of kallikrein 5, a protease involved in the pathophysiology of rosacea, from keratinocytes. Kallikrein 5 that is elevated leads to the production of the LL-37 peptide (cathelicidin).1
Cathelicidin peptide isoforms in rosacea are more plentiful than in normal skin and they also are of different molecular weights and promote angiogenesis. "There are variant forms of cathelicidin that are pro-inflammatory," explains Dr. Gooderham.
Demodex can also lead to disruption of the skin barrier, which can activate TLR2, according to Dr. Gooderham.