Orfali Raquel Leão, Sato Maria Notomi, Takaoka Roberto, Azor Mayce Helena, Rivitti Evandro Ararigbóia, Hanifin Jon M, Aoki Valéria
Department of Dermatology, University of Sao Paulo, School of Medicine, CEP 05403-002, Sao Paulo, Brazil.
Exp Dermatol. 2009 Jul;18(7):628-33. doi: 10.1111/j.1600-0625.2009.00842.x. Epub 2009 Mar 17.
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.
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.
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.
A significant inhibition of the PBMC proliferation response to SEA, PHA, TT and CMA of AD patients was detected (P < or = 0.05). Furthermore, increased levels of IL-18 were detected both in sera and non-stimulated PBMC culture supernatants from AD patients (P < or = 0.05).
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.
特应性皮炎（AD）是一种慢性炎症性皮肤病，患病率高且发病机制复杂。AD患者的皮肤通常被金黄色葡萄球菌（金葡菌）定植；其外毒素可能引发或加重皮肤炎症。多种介质与AD免疫失衡有关，白细胞介素-18（IL-18）作为一种炎症细胞因子，可能在特应性皮肤炎症中起作用。
评估成年AD患者外周血单个核细胞（PBMC）对葡萄球菌肠毒素A（SEA）和B（SEB）的增殖反应以及IL-18水平。
分析了38例成年AD患者和33例健康对照。用SEA、SEB、植物血凝素（PHA）、商陆（PWM）、破伤风类毒素（TT）和白色念珠菌（CMA）刺激PBMC。通过ELISA检测PBMC培养上清液和血清中的IL-18分泌。
检测到AD患者PBMC对SEA、PHA、TT和CMA的增殖反应明显受到抑制（P≤0.05）。此外，在AD患者的血清和未刺激的PBMC培养上清液中均检测到IL-18水平升高（P≤0.05）。
成年AD患者对不同抗原和丝裂原（TT、CMA、SEA和PHA）的PBMC增殖反应降低表明免疫状态受损。AD患者刺激后IL-18的分泌与对照组相似，这可能表明金葡菌维持皮肤炎症的机制不同。另一方面，AD血清和未刺激的细胞培养物中IL-18分泌增加可能会加重AD中观察到的免疫功能障碍，导致皮肤炎症持续存在。
