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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Double-stranded RNA induces production of RANTES and IL-8 by human nasal fibroblasts.
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Double-stranded RNA induces production of RANTES and IL-8 by human nasal fibroblasts.

机译：双链RNA诱导人鼻成纤维细胞产生RANTES和IL-8。

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摘要

Double-stranded RNA (dsRNA) and the viral RNA mimic, polyinosine-polycytidylic acid (poly(I:C)), are recognized by toll-like receptor 3 (TLR3) that mediates the innate immune response to viral infections. In this study, we investigated the effects of poly(I:C) on the production of chemokines (IL-8, RANTES, and eotaxin), Type I IFNs (IFNalpha and IFNbeta), Th1-cytokines (IL-12 and IFNgamma), and pro-inflammatory cytokines (TNF-alpha and IL-1beta) by human nasal mucosa-derived fibroblasts. Human nasal fibroblasts were treated with poly(I:C), and levels of cytokines and chemokines were measured by ELISA. Incubation with poly(I:C) significantly enhanced the secretion of RANTES and IL-8. However, eotaxin, IL-1beta, TNF-alpha, IFNalpha, IFNgamma, and IL-12 were not secreted from nasal fibroblasts stimulated with poly(I:C). The JNK inhibitor SP600125 and the PI3-kinase inhibitor LY294002 significantly blocked the poly(I:C)-induced release of RANTES and IL-8, whereas the p38 MAP kinase inhibitor SB203580 suppressed poly(I:C)-induced secretion of IL-8, but not RANTES. Nasal fibroblasts play an important role in initiating antiviral responses and inflammation of the nasal cavity by producing chemokines leading to enhanced inflammatory cell recruitment.
机译：双链RNA（dsRNA）和病毒RNA类似物聚肌苷-聚胞苷酸（poly（I：C））被通称Toll样受体3（TLR3）识别，该受体介导对病毒感染的先天免疫应答。在这项研究中，我们调查了poly（I：C）对趋化因子（IL-8，RANTES和嗜酸性粒细胞趋化因子），I型干扰素（IFNalpha和IFNbeta），Th1-细胞因子（IL-12和IFNgamma）产生的影响。 ，以及人类鼻粘膜来源的成纤维细胞的促炎性细胞因子（TNF-α和IL-1beta）。用聚（I：C）处理人的鼻成纤维细胞，并通过ELISA测定细胞因子和趋化因子的水平。与poly（I：C）一起孵育可显着增强RANTES和IL-8的分泌。但是，在由poly（I：C）刺激的鼻成纤维细胞中并未分泌嗜酸性粒细胞趋化因子，IL-1β，TNF-α，IFNα，IFNγ和IL-12。 JNK抑制剂SP600125和PI3激酶抑制剂LY294002显着阻断了聚（I：C）诱导的RANTES和IL-8释放，而p38 MAP激酶抑制剂SB203580抑制了聚（I：C）诱导的IL-分泌。 8，但不是RANTES。鼻成纤维细胞通过产生趋化因子导致炎症细胞募集增强，在引发抗病毒反应和鼻腔炎症中起重要作用。

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