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树突状细胞中β2-肾上腺素能受体信号传导减少与佐剂诱导的关节炎大鼠的炎症反应有关。

β2-adrenoceptor signaling reduction in dendritic cells is involved in the inflammatory response in adjuvant-induced arthritic rats.

作者信息

Wu Huaxun, Chen Jingyu, Song Shasha, Yuan Pingfan, Liu Lihua, Zhang Yunfang, Zhou Aiwu, Chang Yan, Zhang Lingling, Wei Wei

机构信息

Institute of Clinical Pharmacology of Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-Inflammatory and Immune Medicine, Hefei, 230032, China.

出版信息

Sci Rep. 2016 Apr 15;6:24548. doi: 10.1038/srep24548.

DOI:10.1038/srep24548
PMID:27079168
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4832233/
Abstract

Rheumatoid arthritis (RA) is characterized by inflammation of the synovium, which leads to the progressive destruction of cartilage and bone. Adrenoreceptor (AR) signaling may play an important role in modulating dendritic cell (DC), which may be involved in the pathogenesis of RA. We examined the effect of the β-AR agonist isoprenaline (ISO) on DC function, the impact of the β2-AR agonist salbutamol on adjuvant-induced arthritic (AA) rats, and changes in β2-AR signaling in DCs during the course of AA. ISO inhibited the expression of the surface molecules CD86 and MHC-II, inhibited the stimulation of T lymphocyte proliferation by DC and TNF-α secretion, and promoted DC antigen uptake and IL-10 secretion. The effects of ISO on MHC-II expression, DC stimulation of T lymphocyte proliferation, and DC antigen uptake were mediated by β2-AR. Treatment with salbutamol ameliorated the severity of AA and histopathology of the joints and inhibited proliferation of thymus lymphocytes and FLS in vivo. β2-AR signaling was weaker in AA rats compared to the control. Elevated GRK2 and decreased β2-AR expression in DC cytomembranes were observed in AA and may have decreased the anti-inflammatory effect of β2-AR signaling. Decreased β2-AR signaling may be relevant to the exacerbation of arthritis inflammation.

摘要

类风湿性关节炎（RA）的特征是滑膜炎症，这会导致软骨和骨骼的渐进性破坏。肾上腺素能受体（AR）信号传导可能在调节树突状细胞（DC）中起重要作用，而树突状细胞可能参与RA的发病机制。我们研究了β-AR激动剂异丙肾上腺素（ISO）对DC功能的影响、β2-AR激动剂沙丁胺醇对佐剂性关节炎（AA）大鼠的影响以及AA病程中DCs中β2-AR信号传导的变化。ISO抑制表面分子CD86和MHC-II的表达，抑制DC对T淋巴细胞增殖的刺激以及TNF-α分泌，并促进DC抗原摄取和IL-10分泌。ISO对MHC-II表达、DC对T淋巴细胞增殖的刺激以及DC抗原摄取的影响是由β2-AR介导的。沙丁胺醇治疗可改善AA的严重程度和关节组织病理学，并在体内抑制胸腺淋巴细胞和FLS的增殖。与对照组相比，AA大鼠的β2-AR信号较弱。在AA中观察到DC细胞膜中GRK2升高和β2-AR表达降低，这可能降低了β2-AR信号传导的抗炎作用。β2-AR信号传导降低可能与关节炎炎症的加重有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/d93517e3d6b8/srep24548-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/04110d99698a/srep24548-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/4c278d3f8e58/srep24548-f2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/0f758da7f2e3/srep24548-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/d93517e3d6b8/srep24548-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/04110d99698a/srep24548-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/4c278d3f8e58/srep24548-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/f31379d671c4/srep24548-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/0f758da7f2e3/srep24548-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4c1/4832233/d93517e3d6b8/srep24548-f5.jpg

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