特应性皮炎增强卵白蛋白诱导小鼠气道炎症的实验研究

目的观察特应性皮炎（AD）的病理变化及其对呼吸道过敏性炎症产生的影响，探讨其形成机制。方法BALB／c小鼠20只，随机分为AD组和丙酮对照组各10只；AD组以7％二硝基氯苯（DNCB）致敏小鼠腹部皮肤，0．5％二硝基氯苯及40恤g鸡卵清蛋白（OVA）激发小鼠背部皮肤；对照组相同时间相同部位涂以丙酮；两组均以1％OVA雾化吸入诱导小鼠气道炎症。观察两组小鼠皮肤及肺部病理改变，收集小鼠支气管肺泡灌洗液（BALF），对BALF进行细胞计数，并用ELISA方法测试BALF及血清中白细胞介素-4（IL-4）、白细胞介素-5（IL-5）、干扰素-γ（IFN-γ）和卵清蛋白IgE（OVA—IgE）含量变化。结果AD组小鼠皮肤病理表现为表皮真皮层增厚，炎症细胞浸润；而对照组皮肤正常。AD组肺部组织炎性细胞较对照组明显增多。BALF中细胞数AD组白细胞总数、中性粒细胞、淋巴细胞及嗜酸性粒细胞增多明显，IL4、IL-5、IFN-γ和OVA—IgE含量均较对照组增高；血清中IL-4、IL-5与OVA．IgE含量较对照组增高。结论特应性皮炎因皮肤受到过敏原刺激能导致全身过敏反应，当吸入同种可溶性抗原时，能使气道炎症加重；其机制可能与Th1／Th2比例失衡，嗜酸性粒细胞、特定性IgE和Th2细胞浸润相关。

Atopic dermatitis enhanced ovalbumin-induced airway inflammation in mice

Objective To observe atopic dermatitis （AD） pathological changes and their influence on aller- gic airway inflammation in order to investigate the mechanism. Methods 20 BALB/c mice were randomly divided in- to the AD group and the control group, and there were 10 in each group. AD group used 7% dinitrochlorobenzene （DNCB） to sensitive mice abdominal skin,with 0.5% dinitrochlorobenzene and 40 μg OVA irritating to mouse back skin, where was coated with acetone in the control group at the same time. All the mice in the two groups were inhaled 1% OVA aerosol inhalation to induce airway inflammation; The mice skin and lung pathological changes were ob- served, and the bronchoalveolar lavage fluid （BALF） was collected and counted. The level of BALF and IL-4, IL-5, IFN-γ and OVA-IgE in serum were tested by ELISA kit. Results Pathological changes in AD mice skin were charac- terized by thickening of epidermis and dermis layer and inflammatory cell infiltration, with no changes in control group. The number of lung inflammatory cells in AD group increased significantly compared with that in the control group. The number of blood WBC, neutrophils,lymphocytes and eosinophils inAD group were significantly increased, and the levels of IL-4, IL-5, IFN-γ and OVA-IgE in both BALF and serumwere increased significantly compared with that in the control group. Conclusions The allergen stimulation to the skin in AD mice could induce systemic aller- gic reactions. The inhale of soluble antigen inhalation could aggravate airway inflammation, which may be involved in the imbalance of Thl/Th2, and infiltration of eosinophils, particular IgE and Th2.