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Serine protease inhibitor lymphoepithelial Kazal type-related inhibitor tends to be decreased in atopic dermatitis.
J. Eur. Acad. Dermatol. Venereol. 23, 1263-1266 (2009)
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.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
1.050
1.050
9
13
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Sprache
englisch
Veröffentlichungsjahr
2009
HGF-Berichtsjahr
0
ISSN (print) / ISBN
0926-9959
e-ISSN
1468-3083
Quellenangaben
Band: 23,
Heft: 11,
Seiten: 1263-1266
Verlag
Wiley
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute for Allergy Research (IAF)
POF Topic(s)
30202 - Environmental Health
Forschungsfeld(er)
Allergy
PSP-Element(e)
G-505400-001
PubMed ID
19522716
Erfassungsdatum
2009-12-31