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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Thymic stromal lymphopoietin receptor-mediated IL-6 and CC/CXC chemokines expression in human airway smooth muscle cells: role of MAPKs (ERK1/2, p38, and JNK) and STAT3 pathways.
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Thymic stromal lymphopoietin receptor-mediated IL-6 and CC/CXC chemokines expression in human airway smooth muscle cells: role of MAPKs (ERK1/2, p38, and JNK) and STAT3 pathways.

机译：胸腺基质淋巴细胞生成素受体介导的IL-6和CC / CXC趋化因子在人气道平滑肌细胞中的表达：MAPK（ERK1 / 2，p38和JNK）和STAT3途径的作用。

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摘要

Thymic stromal lymphopoietin (TSLP) plays a pivotal role in allergic diseases such as asthma, chronic obstructive pulmonary disease, and atopic dermatitis. Enhanced TSLP expression has been detected in asthmatic airways that correlated with both the expression of Th2-attracting chemokines and with disease severity. Although cumulative evidence suggests that human airway smooth muscle (HASM) cells can initiate or perpetuate the airway inflammation by secreting a variety of inflammatory cell products such as cytokines and chemokines, the role of TSLP in this pathway is not known. In the current study, we sought to investigate whether HASM cells express the TSLP receptor (TSLPR) and whether it is functional. We first demonstrated that primary HASM cells express the transcript and protein of both TSLPR subunits (TSLPR and IL-7Ralpha). Functionally, TSLPR-mediated HASM activation induced a significant increase in CXC (IL-8/CXCL8), CC (eotaxin-1/CCL11) chemokines, and proinflammatory cytokine IL-6 expression. Furthermore, using biochemical and genetic approaches, we found that TSLP-induced proinflammatory gene expression in HASM involved the transcriptional mechanisms, MAPKs (ERK1/2, p38, and JNK), and STAT3 activation. Finally, TSLPR immunoreactivity in bronchial sections from mild allergic asthmatics suggested the potential in vivo TSLP targeting of HASM. Altogether, our data suggest that the TSLPR-mediated HASM activation induces proinflammatory cytokine and chemokines release that may facilitate inflammatory immune cells recruitment in airways. In addition, it may be inferred that TSLPR is involved in the pathogenesis of allergic asthma through the activation of HASM cells by TSLP.
机译：胸腺基质淋巴细胞生成素（TSLP）在过敏性疾病（例如哮喘，慢性阻塞性肺疾病和特应性皮炎）中起关键作用。已经在哮喘气道中检测到增强的TSLP表达，其与吸引Th2的趋化因子的表达以及疾病严重性相关。尽管累积证据表明人气道平滑肌（HASM）细胞可以通过分泌多种炎症细胞产物（例如细胞因子和趋化因子）来引发或延续气道炎症，但TSLP在该途径中的作用尚不清楚。在当前的研究中，我们试图调查HASM细胞是否表达TSLP受体（TSLPR）及其功能。我们首先证明原发性HASM细胞表达两个TSLPR亚基（TSLPR和IL-7Ralpha）的转录本和蛋白质。从功能上讲，TSLPR介导的HASM激活诱导CXC（IL-8 / CXCL8），CC（eotaxin-1 / CCL11）趋化因子和促炎性细胞因子IL-6表达显着增加。此外，使用生化和遗传方法，我们发现TSLP诱导的HASM中的促炎基因表达涉及转录机制，MAPK（ERK1 / 2，p38和JNK）和STAT3激活。最后，轻度过敏性哮喘患者支气管切片中的TSLPR免疫反应性提示了靶向TSSM的潜在体内TSLP。总而言之，我们的数据表明，TSLPR介导的HASM激活诱导促炎性细胞因子和趋化因子的释放，这可能促进炎症性免疫细胞在气道中的募集。另外，可以推断TSLPR通过TSLP激活HASM细胞而参与了过敏性哮喘的发病机理。

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