Research Unit of Lung Toxicology (Laboratory of Pneumology), KU Leuven, Leuven, Belgium.
Thorax. 2010 Mar;65(3):252-7. doi: 10.1136/thx.2009.121293.
Persulfate salts are the main cause of occupational asthma (OA) in hairdressers. The aim of this study was to verify whether ammonium persulfate ((NH(4))(2)S(2)O(8), AP) is capable of triggering an asthma-like response in mice.
BALB/c mice were dermally treated on days 1 and 8, with dimethylsulfoxide (DMSO), 1% AP or 5% AP (20 microl/ear). On day 15, the auricular lymph nodes were removed and an in vitro lymphocyte proliferation test (LPT) was performed. AP was tested for its ability to elicit an asthmatic response using a locally developed mouse model of chemical-induced asthma. On days 1 and 8, BALB/c mice received 20 microl AP (5%) or DMSO on each ear. On day 15, they received an intranasal instillation of AP (1%) or saline. Afterwards, ventilatory, inflammatory and immunological parameters were assessed.
The LPT showed that in vitro stimulation of lymphocytes with AP leads to specific proliferation of lymphocytes from AP-sensitised mice. In vivo, AP induced, in AP-sensitised mice only, an 'early' ventilatory response (increased Penh (enhanced pause)) immediately after challenge, and airway hyper-reactivity to methacholine 22 h later. Pulmonary inflammation was mainly characterised by neutrophils (10-15%). AP-sensitised mice showed an increase in total number of T helper (Th) and B lymphocytes together with an increased in vitro secretion of interleukin-4 (IL-4), IL-10 and IL-13 and an increase in total serum immunoglobulin E.
In a mouse model, it was confirmed that dermal sensitisation to AP can lead to asthma-like responses after a single administration via the airway.
过硫酸盐盐是美发师职业性哮喘(OA)的主要原因。本研究旨在验证过硫酸铵((NH 4 ) 2 S 2 O 8 ,AP)是否能在小鼠中引发类似哮喘的反应。
BALB/c 小鼠在第 1 天和第 8 天用二甲基亚砜(DMSO)、1%AP 或 5%AP(20μl/耳)进行皮肤处理。第 15 天,取出耳淋巴结并进行体外淋巴细胞增殖试验(LPT)。使用我们自行开发的化学诱导哮喘小鼠模型,测试 AP 引发哮喘反应的能力。第 1 天和第 8 天,BALB/c 小鼠每只耳朵接受 20μl AP(5%)或 DMSO。第 15 天,它们接受 AP(1%)或生理盐水的鼻腔内滴注。之后,评估通气、炎症和免疫参数。
LPT 显示,AP 体外刺激淋巴细胞导致 AP 致敏小鼠的淋巴细胞特异性增殖。在体内,仅在 AP 致敏小鼠中,AP 诱导“早期”通气反应(在挑战后立即增加 Penh(增强暂停)),并在 22 小时后对乙酰甲胆碱产生气道高反应性。肺部炎症主要表现为中性粒细胞(10-15%)。AP 致敏小鼠显示总 Th 和 B 淋巴细胞数量增加,同时体外分泌白细胞介素-4(IL-4)、IL-10 和 IL-13 增加,总血清免疫球蛋白 E 增加。
在小鼠模型中,证实了通过气道单次给药后,AP 皮肤致敏可导致类似哮喘的反应。