高温和低温加重哮喘的气道炎症：来自小鼠模型中的证据
2019/12/09
摘要
流行病学表明，环境温度是哮喘的诱因和潜在激活剂。高温和低温在哮喘气道炎症中的作用以及潜在的分子机制尚不清楚。我们实验采用了哮喘小鼠模型。在工作日，将BALB / c小鼠在不同温度下暴露4 h（早晨2 h和下午2 h）。暴露温度为10℃，24℃和40℃。在第14、18、22、26和30天使用卵清蛋白（OVA）致敏小鼠，第32-38天开始进行气雾刺激30分钟。最后一次OVA激发后，评估肺功能，血清蛋白和肺部炎症。在24°C比较OVA组和生理盐水组，我们发现血清总IgE（p<0.05）； OVA-sIgE（p <0.01）; IL-4（p <0.05）; IL-1β（p <0.01）; IL-6（p <0.01）;THF -α（p <0.01）; IL-4 /IFN-γ之比（p <0.01）显著增加。同时，IFN-γ明显降低（p <0.01）。随着温度的升高，免疫蛋白和促炎因子呈U形，在24°C时达到峰值，但IFN-γ除外（倒U形）。与24°C组相比，高温和低温暴露后，Ri和Re显著增加，而Cldyn显著降低。 OVA组的组织病理学分析显示气道重塑，气道壁增厚和变形以及上皮下纤维化。在高温和低温暴露组中发现了更明显的变化。免疫组化提示TRPs随温度变化而变化。高温和低温会加剧哮喘小鼠模型的气道炎症。TRPs在过敏性哮喘的温度加重中起重要作用。结果表明，哮喘患者应避免长时间暴露在高温和低温环境。
High and low temperatures aggravate airway inflammation of asthma: Evidence in a mouse model.
Deng L, Ma P, Wu Y, Ma Y, Yang X, Li Y, Deng Q.
Abstract
Epidemiology suggests ambient temperature is the triggers and potential activator of asthma. The role of high and low temperatures on airway inflammation of asthma, and the underlying molecular mechanism are not yet understood. A mouse model of asthma was adopted in our experiment. The BALB/c mice were exposed at different temperature for 4 h (2 h in the morning and 2 h in the afternoon) on weekday. The exposure temperatures were 10 °C, 24 °C and 40 °C. Ovalbumin (OVA) was used to sensitize the mice on days 14, 18, 22, 26, and 30, followed by an aerosol challenge for 30 min from day 32-38. After the final OVA challenge, lung function, serum protein and pulmonary inflammation were assessed. Comparing the OVA with the saline group at 24 °C, we saw a significant increase in: serum Total-IgE (p < 0.05); OVA-sIgE (p < 0.01); IL-4 (p < 0.05); IL-1β (p < 0.01); IL-6 (p < 0.01); TNF-α (p < 0.01); and the ratio of IL-4/IFN-γ (p < 0.01). At the same time, there was a significant decrease in IFN-γ (p < 0.01). As the temperature increase, there is a U shape for immune proteins and pro-inflammatory factors with a peak value at 24 °C, exception for IFN-γ (inverted U-shape). After the high and low temperature exposure, the Ri and Re increased significantly, while Cldyn decreased significantly compared with the 24 °C group. Histopathological analysis of the OVA groups showed airway remodeling, airway wall thickening and deforming, and subepithelial fibrosis. More obvious changes were found in the high and low temperature exposure groups. The immunohistochemistry suggested that TRPs changed with temperatures. High and low temperatures can aggravate airway inflammation in a mouse model of asthma. TRPs play an important role in temperature aggravation of allergic asthma. The results suggest that asthmatics should avoid exposure to high and low temperatures for too long time.
流行病学表明，环境温度是哮喘的诱因和潜在激活剂。高温和低温在哮喘气道炎症中的作用以及潜在的分子机制尚不清楚。我们实验采用了哮喘小鼠模型。在工作日，将BALB / c小鼠在不同温度下暴露4 h（早晨2 h和下午2 h）。暴露温度为10℃，24℃和40℃。在第14、18、22、26和30天使用卵清蛋白（OVA）致敏小鼠，第32-38天开始进行气雾刺激30分钟。最后一次OVA激发后，评估肺功能，血清蛋白和肺部炎症。在24°C比较OVA组和生理盐水组，我们发现血清总IgE（p<0.05）； OVA-sIgE（p <0.01）; IL-4（p <0.05）; IL-1β（p <0.01）; IL-6（p <0.01）;THF -α（p <0.01）; IL-4 /IFN-γ之比（p <0.01）显著增加。同时，IFN-γ明显降低（p <0.01）。随着温度的升高，免疫蛋白和促炎因子呈U形，在24°C时达到峰值，但IFN-γ除外（倒U形）。与24°C组相比，高温和低温暴露后，Ri和Re显著增加，而Cldyn显著降低。 OVA组的组织病理学分析显示气道重塑，气道壁增厚和变形以及上皮下纤维化。在高温和低温暴露组中发现了更明显的变化。免疫组化提示TRPs随温度变化而变化。高温和低温会加剧哮喘小鼠模型的气道炎症。TRPs在过敏性哮喘的温度加重中起重要作用。结果表明，哮喘患者应避免长时间暴露在高温和低温环境。
(中日友好医院呼吸与危重症医学科 王瑞茵 摘译 林江涛 审校)
(Environ Pollut. 2019 Nov 13:113433. doi: 10.1016/j.envpol.2019.113433. [Epub ahead of print])
(Environ Pollut. 2019 Nov 13:113433. doi: 10.1016/j.envpol.2019.113433. [Epub ahead of print])
High and low temperatures aggravate airway inflammation of asthma: Evidence in a mouse model.
Deng L, Ma P, Wu Y, Ma Y, Yang X, Li Y, Deng Q.
Abstract
Epidemiology suggests ambient temperature is the triggers and potential activator of asthma. The role of high and low temperatures on airway inflammation of asthma, and the underlying molecular mechanism are not yet understood. A mouse model of asthma was adopted in our experiment. The BALB/c mice were exposed at different temperature for 4 h (2 h in the morning and 2 h in the afternoon) on weekday. The exposure temperatures were 10 °C, 24 °C and 40 °C. Ovalbumin (OVA) was used to sensitize the mice on days 14, 18, 22, 26, and 30, followed by an aerosol challenge for 30 min from day 32-38. After the final OVA challenge, lung function, serum protein and pulmonary inflammation were assessed. Comparing the OVA with the saline group at 24 °C, we saw a significant increase in: serum Total-IgE (p < 0.05); OVA-sIgE (p < 0.01); IL-4 (p < 0.05); IL-1β (p < 0.01); IL-6 (p < 0.01); TNF-α (p < 0.01); and the ratio of IL-4/IFN-γ (p < 0.01). At the same time, there was a significant decrease in IFN-γ (p < 0.01). As the temperature increase, there is a U shape for immune proteins and pro-inflammatory factors with a peak value at 24 °C, exception for IFN-γ (inverted U-shape). After the high and low temperature exposure, the Ri and Re increased significantly, while Cldyn decreased significantly compared with the 24 °C group. Histopathological analysis of the OVA groups showed airway remodeling, airway wall thickening and deforming, and subepithelial fibrosis. More obvious changes were found in the high and low temperature exposure groups. The immunohistochemistry suggested that TRPs changed with temperatures. High and low temperatures can aggravate airway inflammation in a mouse model of asthma. TRPs play an important role in temperature aggravation of allergic asthma. The results suggest that asthmatics should avoid exposure to high and low temperatures for too long time.
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