EXPRESSION OF EPIDERMAL CAMP CHANGES IN PARALLEL WITH PERMEABILITY BARRIER STATUS

Two critical defensive functions of the outer epidermis, the permeability barrier and antimicrobial defense, share certain structural and biochemical features. Moreover, 3antimicrobial peptides (AMP); i.e., mouse beta-defensin 3 (mBD3), mouse cathelicidin protein (mCAMP), and the neuroendocrine peptide, catestatin, all localize to the outer epidermis, and both mBD3 and mCAMP are secreted from epidermal lamellar bodies with other organelle contents that subserve the permeability barrier. These 3 AMP are up-regulated in response to acute permeability barrier disruption, while conversely, mCAMP−/ − mice (unable to combatgram-positive pathogens) also display abnormal barrier homeostasis. To determine further whether these two functions are co-regulated, we investigated changes in immunostaining for these 3 AMP in skin samples in which permeability barrier function in mice had been either compromised or enhanced. Compromised or enhanced barrier function correlated with reduced or enhanced immunohistochemical expression of mCAMP, respectively, but conversely with Cst expression likely due to the role of this AMP as an endogenous inhibitor of cathelicidin expression. mBD3 expression correlated with experimental barrier perturbations, but poorly with developmental changes in barrier function