D Roedl1, C Traidl-Hoffmann, J Ring, H Behrendt, M Braun-Falco. 1. ZAUM-Center for Allergy and Environment, Division of Environmental Dermatology and Allergy, Helmholz Zentrum München, Technische Universität München, Munich, Germany.
Abstract
BACKGROUND: A pathogenic role of serine protease inhibitor lymphoepithelial Kazal type-related inhibitor (LEKTI) in atopic dermatitis (AD) is currently in intense debate. Analyses of an association between genetic polymorphisms of SPINK5 and atopic diseases revealed contradictory results. Herein, we assessed the role of LEKTI in AD at an expressional and functional level. METHODS: The expression of LEKTI and its inhibitory capacity was measured by real-time polymerase chain reaction and hydrolytic activity assay, respectively, in keratinocyte cell cultures of three AD patients in comparison to cultures of healthy individuals (5x) and Netherton (NS) patients (3x). RESULTS: Expression of LEKTI was significantly decreased in AD vs. healthy volunteers. Due to reduced protease inhibition, trypsin-like hydrolytic activity in AD was slightly increased, although not significantly. CONCLUSIONS: Even though the number of investigated subjects was small and hydrolytic activity was only slightly increased, the results denote that LEKTI might be diminished in AD. The study also disclosed the necessity of functional analyses in addition to genetic investigations to gain further and more detailed insights into the role of LEKTI in AD.
BACKGROUND: A pathogenic role of serine protease inhibitor lymphoepithelial Kazal type-related inhibitor (LEKTI) in atopic dermatitis (AD) is currently in intense debate. Analyses of an association between genetic polymorphisms of SPINK5 and atopic diseases revealed contradictory results. Herein, we assessed the role of LEKTI in AD at an expressional and functional level. METHODS: The expression of LEKTI and its inhibitory capacity was measured by real-time polymerase chain reaction and hydrolytic activity assay, respectively, in keratinocyte cell cultures of three ADpatients in comparison to cultures of healthy individuals (5x) and Netherton (NS) patients (3x). RESULTS: Expression of LEKTI was significantly decreased in AD vs. healthy volunteers. Due to reduced protease inhibition, trypsin-like hydrolytic activity in AD was slightly increased, although not significantly. CONCLUSIONS: Even though the number of investigated subjects was small and hydrolytic activity was only slightly increased, the results denote that LEKTI might be diminished in AD. The study also disclosed the necessity of functional analyses in addition to genetic investigations to gain further and more detailed insights into the role of LEKTI in AD.