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COX-2 induces T cell accumulation and IFN-γ production during the development of chromium allergy.
Autoimmunity ( IF 3.3 ) Pub Date : 2019-10-06 , DOI: 10.1080/08916934.2019.1662404
Ratri Maya Sitalaksmi 1, 2, 3 , Koyu Ito 1 , Kouetsu Ogasawara 1 , Yoshiko Suto 1 , Madoka Itabashi 1 , Kyosuke Ueda 4 , Noriyasu Hirasawa 5 , Takayuki Narushima 4 , Nike Hendrijantini 3 , Utari Kresnoadi 3 , Keiichi Sasaki 2
Affiliation  

Chromium (Cr) is commonly added into various metal alloys to improve some mechanical properties such as corrosion resistance, strength, and workability. However, Cr is also known to be a metal allergen for some individuals. Metal allergy is a T cell-mediated disease with symptoms of inflammation and swelling that involve inflammatory cytokines and prostaglandins. Hence, suppressing these inflammation paths by using COX-2 inhibitor might be useful in treating Cr allergy. In this study, mice were used with Cr-induced allergy challenge model. The mice were injected with celecoxib once per day for 7 days one hour after the challenge. Footpad samples were stained with haematoxylin and eosin (H&E), and lymphocytes were isolated from popliteal lymph nodes for the flow cytometric analysis. The results show that both prostaglandin E2 (PGE2), a known mediator of inflammation, and cyclooxygenases (COX)-2 have important roles in the development of Cr allergy. Further, COX-2 inhibitor, celecoxib, was effective in relieving swelling and inflammation in Cr-allergic mice concordant with suppression of IFN-γ production by CD8+ T cells and T cell accumulation in the lymph nodes. Therefore, the inhibition of COX-2 may be a therapeutic target for Cr allergy, and additional molecules in the PGE2 signalling pathway may also be an effective therapeutic target for the treatment of metal allergy.

中文翻译:

在铬过敏发生期间,COX-2诱导T细胞积累和IFN-γ产生。

铬(Cr)通常添加到各种金属合金中,以改善某些机械性能,例如耐腐蚀性,强度和可加工性。但是,对于某些人来说,铬也是一种金属过敏原。金属过敏是由T细胞介导的疾病,具有炎症和肿胀症状,涉及炎症细胞因子和前列腺素。因此,通过使用COX-2抑制剂抑制这些炎症路径可能对治疗Cr过敏有用。在这项研究中,小鼠与Cr诱发的过敏反应模型一起使用。攻击后一小时,每天一次给小鼠注射塞来昔布,持续7天。足垫样品用苏木精和曙红(H&E)染色,并从pop淋巴结中分离淋巴细胞用于流式细胞仪分析。结果表明,前列腺素E2(PGE2),已知的炎症介质,环氧合酶(COX)-2在Cr过敏的发生中起重要作用。此外,COX-2抑制剂塞来昔布可有效缓解Cr过敏小鼠的肿胀和炎症,这与抑制CD8 + T细胞产生的IFN-γ和抑制T细胞在淋巴结中的蓄积有关。因此,抑制COX-2可能是Cr过敏的治疗靶标,PGE2信号通路中的其他分子也可能是治疗金属过敏的有效治疗靶标。可以有效缓解Cr过敏小鼠的肿胀和炎症,这与抑制CD8 + T细胞产生的IFN-γ和T细胞在淋巴结中的蓄积有关。因此,抑制COX-2可能是Cr过敏的治疗靶标,PGE2信号传导途径中的其他分子也可能是治疗金属过敏的有效治疗靶标。可以有效缓解Cr过敏小鼠的肿胀和炎症,这与抑制CD8 + T细胞产生的IFN-γ和T细胞在淋巴结中的蓄积有关。因此,抑制COX-2可能是Cr过敏的治疗靶标,PGE2信号通路中的其他分子也可能是治疗金属过敏的有效治疗靶标。
更新日期:2019-11-01
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