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白细胞介素-33促进小鼠角质形成细胞衍生趋化因子(一种白细胞介素-8同系物)在卵清蛋白致敏小鼠气道平滑肌细胞中的表达。

IL-33 promotes mouse keratinocyte-derived chemokine, an IL-8 homologue, expression in airway smooth muscle cells in ovalbumin-sensitized mice.

作者信息

Wu Wei, Xu Yuzhu, He Xinliang, Lu Yan, Guo Yali, Yin Zhuoran, Xie Jungang, Zhao Jianping

机构信息

Department of Respiratory and crit care , Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

出版信息

Asian Pac J Allergy Immunol. 2014 Dec;32(4):337-44. doi: 10.12932/AP0450.32.4.2014.

DOI:10.12932/AP0450.32.4.2014
PMID:25543045
Abstract

BACKGROUND

Although it is recognized that IL-33 plays a key role in the onset of asthma, it is currently unclear whether IL-33 acts on any other target cells besides mast cells and Th2 cells in asthma. We investigated that whether airway smooth muscle cells (ASMCs) could contribute to asthma via stimulation with IL-33.

METHODS

To create a mouse model of acute asthma, murine ASMCs were isolated and cultured in vitro with IL-33. The ASMCs were divided into two groups, ASMCs from normal mice and ASMCs from ovalbumin-sensitized mice. The release of mouse KC was analyzed by PCR and ELISA. Immunocytochemical Staining of murine ASMCs for ST2 and IL-1RAcP was performed.

RESULTS

IL-33 promoted KC expression, both in terms of mRNA and protien levels, in ASMCs from ovalbumin-sensitized mice. ST2 and IL-1RAcP were expressed in the membrane of ASMCs in ovalbumin-sensitized mice.

CONCLUSION

IL-33 may contribute to the inflammation in the airways by acting on airway smooth muscle cells. IL-33 and ST2 may play important roles in allergic bronchial asthma.

摘要

背景

尽管人们认识到白细胞介素-33(IL-33)在哮喘发病中起关键作用,但目前尚不清楚在哮喘中,IL-33除作用于肥大细胞和辅助性T2(Th2)细胞外,是否还作用于其他靶细胞。我们研究了气道平滑肌细胞(ASMCs)是否会通过IL-33刺激而导致哮喘。

方法

为建立急性哮喘小鼠模型,分离小鼠ASMCs并在体外与IL-33一起培养。将ASMCs分为两组,正常小鼠的ASMCs和卵清蛋白致敏小鼠的ASMCs。通过聚合酶链反应(PCR)和酶联免疫吸附测定(ELISA)分析小鼠趋化因子(KC) 的释放。对小鼠ASMCs进行ST2和白细胞介素-1受体拮抗剂(IL-1RAcP)的免疫细胞化学染色。

结果

IL-33促进了卵清蛋白致敏小鼠的ASMCs中KC的表达,无论是在mRNA水平还是蛋白水平。ST2和IL-1RAcP在卵清蛋白致敏小鼠的ASMCs膜中表达。

结论

IL-33可能通过作用于气道平滑肌细胞而导致气道炎症。IL-33和ST2可能在过敏性支气管哮喘中起重要作用。

相似文献

1
IL-33 promotes mouse keratinocyte-derived chemokine, an IL-8 homologue, expression in airway smooth muscle cells in ovalbumin-sensitized mice.白细胞介素-33促进小鼠角质形成细胞衍生趋化因子(一种白细胞介素-8同系物)在卵清蛋白致敏小鼠气道平滑肌细胞中的表达。
Asian Pac J Allergy Immunol. 2014 Dec;32(4):337-44. doi: 10.12932/AP0450.32.4.2014.
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Exchange protein directly activated by cAMP (Epac) protects against airway inflammation and airway remodeling in asthmatic mice.环磷酸腺苷(cAMP)直接激活的交换蛋白(Epac)可预防哮喘小鼠的气道炎症和气道重塑。
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IL-33 induces Th17-mediated airway inflammation via mast cells in ovalbumin-challenged mice.IL-33 通过肥大细胞诱导卵清蛋白激发的小鼠 Th17 介导的气道炎症。
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Blockade of IL-33/ST2 ameliorates airway inflammation in a murine model of allergic asthma.在过敏性哮喘小鼠模型中,阻断白细胞介素-33/ST2可改善气道炎症。
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IL-33 amplifies the polarization of alternatively activated macrophages that contribute to airway inflammation.白细胞介素-33增强了交替活化巨噬细胞的极化,而这种极化会导致气道炎症。
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Interleukin-33 and alveolar macrophages contribute to the mechanisms underlying the exacerbation of IgE-mediated airway inflammation and remodelling in mice.白细胞介素-33 和肺泡巨噬细胞有助于介导 IgE 气道炎症和重塑的机制在小鼠中的加重。
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