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Microanalysis of an antimicrobial peptide, β‐defensin‐2, in the stratum corneum from patients with atopic dermatitis
Author(s) -
Asano S.,
Ichikawa Y.,
Kumagai T.,
Kawashima M.,
Imokawa G.
Publication year - 2008
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2008.08613.x
Subject(s) - beta defensin , stratum corneum , defensin , antimicrobial peptides , staphylococcus aureus , atopic dermatitis , staphylococcal skin infections , antimicrobial , immunology , microbiology and biotechnology , cathelicidin , medicine , biology , skin infection , pathology , bacteria , genetics
Summary Background Antimicrobial peptides, such as defensin and cathelicidin, have recently been reported to play important roles in host defence and in cutaneous innate immunity. Although β‐defensin‐2 has been reported to be downregulated in the skin of patients with atopic dermatitis (AD), little is known about its role in the colonization of Staphylococcus aureus in the stratum corneum of patients with AD. A precise evaluation of these peptides in the stratum corneum as an antimicrobial barrier against S. aureus colonization has not yet been performed. Objectives To compare β‐defensin‐2 levels in the skin of patients with AD and healthy controls. Methods We developed a microanalytical technique to measure β‐defensin‐2 in the stratum corneum using a combination of immunoprecipitation and Western blotting. Results β‐Defensin‐2 in the stratum corneum was significantly higher in AD lesional skin compared with healthy control skin. The β‐defensin‐2 content in AD lesional skin also increased in proportion to the severity of the disease. Counting bacterial colonies revealed higher populations of S. aureus on lesional and nonlesional skin surfaces of patients with AD compared with healthy controls. Comparison of S. aureus colony numbers and β‐defensin‐2 levels demonstrated a positive correlation ( r = 0·342, P = 0·004, n = 67) between both factors. Conclusions Collectively, these findings suggest that β‐defensin‐2 is induced in response to bacteria, injury or inflammatory stimuli and is not associated with vulnerability to S. aureus colonization in the skin of patients with AD.