Atopic dermatitis in adults: evaluation of peripheral blood mononuclear cells proliferation response to Staphylococcus aureus enterotoxins A and B and analysis of interleukin‐18 secretion

外周血单个核细胞 金黄色葡萄球菌 特应性皮炎 肠毒素 免疫学 分泌物 外周血 医学 超抗原 微生物学 白细胞介素 生物 免疫系统 细胞因子 T细胞 细菌 体外 内科学 大肠杆菌 基因 生物化学 遗传学
作者
Raquel Leão Orfali,Maria Notomi Sato,Roberto Takaoka,Mayce Helena Azor,Evandro A. Rivitti,Jon M. Hanifin,Valéria Aoki
出处
期刊:Experimental Dermatology [Wiley]
卷期号:18 (7): 628-633 被引量:32
标识
DOI:10.1111/j.1600-0625.2009.00842.x
摘要

Abstract: Background: Atopic dermatitis (AD) is a chronic, inflammatory skin disease with a high prevalence and complex pathogenesis. The skin of AD patients is usually colonized by Staphylococcus aureus ( S. aureus ); its exotoxins may trigger or enhance the cutaneous inflammation. Several mediators are related to the AD immune imbalance and interleukin‐18 (IL‐18), an inflammatory cytokine, may play a role in the atopic skin inflammation. Aims: To evaluate peripheral blood mononuclear cells (PBMC) proliferation response to staphylococcal enterotoxins A (SEA) and B (SEB) and the levels of IL‐18 in adults with AD. Methods: Thirty‐eight adult patients with AD and 33 healthy controls were analysed. PBMC were stimulated with SEA and SEB, phytohemaglutinin (PHA), pokeweed (PWM), tetanus toxoid (TT) and Candida albicans (CMA). IL‐18 secretion from PBMC culture supernatants and sera were measured by ELISA. Results: A significant inhibition of the PBMC proliferation response to SEA, PHA, TT and CMA of AD patients was detected ( P ≤ 0.05). Furthermore, increased levels of IL‐18 were detected both in sera and non‐stimulated PBMC culture supernatants from AD patients ( P ≤ 0.05). Conclusions: A decreased PBMC proliferation response to distinct antigens and mitogens (TT, CMA, SEA and PHA) in adults with AD suggest a compromised immune profile. IL‐18 secretion from AD upon stimulation was similar from controls, which may indicate a diverse mechanism of skin inflammation maintained by Staphylococcus aureus. On the other hand, augmented IL‐18 secretion from AD sera and non‐stimulated cell culture may enhance the immune dysfunction observed in AD, leading to constant skin inflammation.

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