For over two thousand years blistering beetles and their extracts have been used to remove noxious, noisome, persistent warts from skin. Research through 1960 (yes, before many of us were born), before keratinocyte culture, before PCR, before demonstrating autoantibodies in Pemphigus and Pemphigoid, was reviewed and worth a read, since it may yield clues pertinent even today (Bagatell & Stoughton, 1964).
Fast forward to last month.
At the Society for Investigative Dermatology meeting in Atlanta in May 2015, Li et al reported fascinating research in cultured human keratinocytes. Cantharidin, the active blistering component of blister beetle juice, specifically cleaved desmocollin (DSC) 2/3 both extracellularly and intracellularly, and DSC ectodomain fragments appeared in the culture media.. Even more interesting was that cantharidin caused intracellular cleavage of DSC . The extracellular cleavage was blocked by metalloprotease inhibitors, and a tyrosine kinase inhibitor, genistin, blocked both the extracellular and intracellular cleavage of DSC 2/3. Those interested in tyrosine kinases may let their imaginations run wild concerning new wart therapies.
Another major question beyond these very interesting mechanistic findings is whether the mechanism of acantholysis caused by cantharidin is a clue to the mechanism of acantholysis in some of the autoimmune blistering diseases.
Bagatell, F and Stoughton RB (1964) Vesication and Acantholysis chapter XXXI, in The Epidermis W. Montagna and WC Lobitz eds. Academic Press, NY, NY, pages 601-611.
Li, N, Liu, Z, Diaz, LA (2015) Desmocollin ectodomain shedding and cantharidin acantholysis Abstract Number 382, J Invest Derm 135:S65, 2015, page S65 (Abstract Number 382).
Conflict of Interest:
Your blogger in an Emeritus professor at UNC Chapel Hill where this research was conducted but had no role in the research.