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Expression of antimicrobial peptides in the normal and involved skin of patients with infective cellulitis.
J Infect Dis ; 196(9): 1425-30, 2007 Nov 01.
Article em En | MEDLINE | ID: mdl-17922409
BACKGROUND: Endogenous antimicrobial peptides participate in the innate defense of skin against a variety of pathogens. The systemic expression of these peptides in normal-appearing skin of patients with infective cellulitis is unknown. METHODS: Study patients were adults with infective cellulitis and signs of systemic inflammation. Skin biopsy and serum specimens were obtained from patients and from control subjects with no active infection. Cathelicidin and human beta-defensin 2 mRNA expression were determined by real-time polymerase chain reaction. RESULTS: Skin biopsy specimens from 11 patients and 4 uninfected control subjects were analyzed. The relative expression level for cathelicidin mRNA was elevated in both the involved and the distal normal-appearing skin of patients with cellulitis, compared with expression in the skin of control subjects (mean ratios, 39.46 vs. 1.32, P=.0059; and 21.41 vs. 1.32, P=.0059). Similarly, the relative expression level of human beta -defensin 2 mRNA was elevated in both the involved skin (mean ratios, 20,844 vs. 11.65; P=.0015) and in distal normal-appearing skin of patients with cellulitis (mean ratios, 201.1 vs. 11.65; P=.0103). DISCUSSION: In response to cutaneous infection there is a local and distal increase in endogenous antimicrobial peptide mRNA in both involved and normal-appearing skin. These observations show, for the first time to our knowledge, that after infection the human body responds by increasing systemic innate immunity.
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Base de dados: MEDLINE Assunto principal: Celulite (Flegmão) / Peptídeos Catiônicos Antimicrobianos / Beta-Defensinas Idioma: En Ano de publicação: 2007 Tipo de documento: Article
Buscar no Google
Base de dados: MEDLINE Assunto principal: Celulite (Flegmão) / Peptídeos Catiônicos Antimicrobianos / Beta-Defensinas Idioma: En Ano de publicação: 2007 Tipo de documento: Article