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变应性哮喘小鼠模型中与性别相关的脾细胞功能

Sex-related splenocyte function in a murine model of allergic asthma.

作者信息

Okuyama K, Wada K, Chihara J, Takayanagi M, Ohno I

机构信息

Department of Pathophysiology, Tohoku Pharmaceutical University, Sendai, Japan.

出版信息

Clin Exp Allergy. 2008 Jul;38(7):1212-9. doi: 10.1111/j.1365-2222.2008.03015.x. Epub 2008 May 21.

Abstract

BACKGROUND

The prevalence and severity of asthma are higher among boys than girls, but the ratios are reversed after puberty. These observations strongly suggest that sex hormones have a role in the pathogenesis of the disease. However, the mechanisms underlying the gender differences in asthma are not fully understood.

OBJECTIVE

The aim of this study was to investigate sex differences in allergic inflammation in terms of immune function.

METHODS

Male and female C57BL/6 mice were sensitized and challenged with ovalbumin (OVA). OVA-specific IgE in serum and airway inflammation were compared between sexes. Splenocytes from OVA-sensitized male or female donor mice were transferred to male or female naïve recipient mice. Subsequently, the recipient mice were challenged, followed by the evaluation of OVA-specific IgE and airway inflammation. Cytokines secreted from splenocytes of the sensitized mice were measured.

RESULTS

The levels of OVA-specific IgE and the allergen-induced airway inflammation were higher in female than in the male mice. The contents of T-helper type 2 (Th2) cytokines, IL-4, IL-5 and IL-13, in the bronchoalveolar lavage fluid from female mice were higher than those from male mice. The airway inflammation in female recipients transferred with splenocytes from female donors was more severe than that in any other combination of recipients and donors. Splenocytes from the sensitized female mice produced more of the Th2 cytokine, IL-5, than those from the sensitized male mice upon stimulation with OVA.

CONCLUSION

Our findings suggest that the sex difference in allergic airway inflammation may be attributable to the sex difference in not only the hormonal environment but also in the immune cells themselves.

摘要

背景

哮喘的患病率和严重程度在男孩中高于女孩,但在青春期后这种比例会逆转。这些观察结果强烈表明性激素在该疾病的发病机制中起作用。然而,哮喘性别差异背后的机制尚未完全了解。

目的

本研究的目的是从免疫功能方面研究变应性炎症中的性别差异。

方法

将雄性和雌性C57BL/6小鼠用卵清蛋白(OVA)致敏并激发。比较两性血清中OVA特异性IgE和气道炎症情况。将OVA致敏的雄性或雌性供体小鼠的脾细胞转移至雄性或雌性未致敏的受体小鼠。随后,对受体小鼠进行激发,接着评估OVA特异性IgE和气道炎症。检测致敏小鼠脾细胞分泌的细胞因子。

结果

雌性小鼠中OVA特异性IgE水平和变应原诱导的气道炎症高于雄性小鼠。雌性小鼠支气管肺泡灌洗液中2型辅助性T(Th2)细胞因子IL-4、IL-5和IL-13的含量高于雄性小鼠。接受来自雌性供体脾细胞转移的雌性受体小鼠的气道炎症比受体和供体的任何其他组合都更严重。在用OVA刺激后,致敏雌性小鼠的脾细胞比致敏雄性小鼠的脾细胞产生更多的Th2细胞因子IL-5。

结论

我们的研究结果表明,变应性气道炎症中的性别差异可能不仅归因于激素环境的性别差异,还归因于免疫细胞本身的性别差异。

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