Differential susceptibility of Cx26 mutations associated with epidermal dysplasias to peptidoglycan derived from Staphylococcus aureus and Staphylococcus epidermidis

Steven Donnelly, Grant English, Eugene A. de Zwart-Storm, Susan Lang, Maurice A.M. van Steensel, Patricia E. Martin

Research output: Contribution to journalArticle


Mutations in Connexin26 (Cx26) give rise to a spectrum of dominantly inherited hyperproliferating skin disorders, the severest being keratitis–ichthyosis–deafness (KID) syndrome, an inflammatory skin disorder, with patients prone to opportunistic infections. We compared the effects of peptidoglycan (PGN) extracted from the skin commensal Staphylococcus epidermidis and the opportunistic pathogen Staphylococcus aureus on interleukin-6 and connexin expression in HaCaT cells (a keratinocyte cell line) and connexin channel activity in HaCaT and HeLa (connexin deficient) cells transfected to express KID and non-KID Cx26 mutations.
Original languageEnglish
Pages (from-to)592-598
Number of pages7
JournalExperimental Dermatology
Issue number8
Early online date29 May 2012
Publication statusPublished - Aug 2012



  • epidermal dysplasia
  • peptidoglycan
  • Staphylococcus aureus
  • Staphylococcus epidermidis

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