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寄生虫感染抑制气道过敏反应,树突状细胞参与调节过程。

Helminth infection inhibits airway allergic reaction and dendritic cells are involved in the modulation process.

机构信息

School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300072, P. R. China.

出版信息

Parasite Immunol. 2010 Jan;32(1):57-66. doi: 10.1111/j.1365-3024.2009.01161.x.

Abstract

Several previous studies have demonstrated that some helminth infections can inhibit allergic reactions, but the examination on the effect of live Schistosoma japonicum (SJ) infection on allergic inflammation remains limited. The aim of this study was to examine the effect and mechanism of chronic SJ infection on airway allergic inflammation in a murine model. The data showed that chronic SJ infection suppressed airway eosinophilia, mucus production and antigen-specific IgE responses induced by ovalbumin (OVA) sensitization and challenge. Cytokine production analysis showed that chronic SJ infection reduced allergen-driven interleukin (IL)-4 and IL-5 production, but had no significant effect on IFN-gamma production. More importantly, we found that the adoptive transfer of dendritic cells (DCs) from SJ-infected mice dramatically decreased airway allergic inflammation in the recipients, which was associated with significant decrease of IL-4/IL-5 production and increase of IL-10 production. The results suggest that SJ infection may inhibit the development of allergy and that DCs may be involved in the process of helminth infection-mediated modulation of allergic inflammation.

摘要

已有多项研究表明,某些寄生虫感染可以抑制过敏反应,但活日本血吸虫(SJ)感染对过敏炎症影响的研究仍然有限。本研究旨在探讨慢性 SJ 感染对卵清蛋白(OVA)致敏和激发诱导的小鼠气道过敏性炎症的影响及机制。结果显示,慢性 SJ 感染抑制了由 OVA 致敏和激发诱导的气道嗜酸性粒细胞增多、黏液产生和抗原特异性 IgE 反应。细胞因子产生分析表明,慢性 SJ 感染减少了变应原驱动的白细胞介素(IL)-4 和 IL-5 的产生,但对 IFN-γ的产生没有显著影响。更重要的是,我们发现从 SJ 感染小鼠过继转移树突状细胞(DC)可显著降低受者的气道过敏性炎症,这与 IL-4/IL-5 产生的显著减少和 IL-10 产生的增加有关。结果表明,SJ 感染可能抑制过敏的发生,而 DC 可能参与了寄生虫感染介导的过敏炎症调节过程。

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