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阿司匹林加重性呼吸道疾病中阿司匹林脱敏治疗前后细胞因子表达。

Cytokine expression before and after aspirin desensitization therapy in aspirin-exacerbated respiratory disease.

机构信息

Division of Allergy and Immunology, Department of Internal Medicine, Celal Bayar University School of Medicine, Manisa, Turkey,

出版信息

Inflammation. 2013 Dec;36(6):1553-9. doi: 10.1007/s10753-013-9699-7.

Abstract

Aspirin exacerbated respiratory disease (AERD) is induced by acetylsalicylic acid (ASA) and/or nonsteroidal antiinflammatory drugs (NSAIDs). Effects of desensitization on many mediators have been examined previously, but few studies addressed the influence of desensitization on T lymphocytes and T lymphocyte-derived cytokines. This study was performed to examine peripheral blood lymphocyte (PBL) cytokine expression in aspirin-sensitive patients who have asthma before and after aspirin desensitization. In this study, the release of interleukin-2 (IL-2), interleukin-4 (IL-4), and interferon-gamma (IFN-γ) by CD4+ T lymphocytes prior to aspirin desensitization were also measured at intracellular levels, and expression of these cytokines after 1 month aspirin desensitization was evaluated. Twelve patients with AERD were included in the study. Two different control groups were formed, one consisted of 15 healthy people and second 12 aspirin tolerant asthmatic (ATA) patients using aspirin. A blood sample was collected prior to desensitization, and the tests were repeated by taking a second blood sample 1 month after the 4-day desensitization treatment. The proportion of lymphocytes secreting IFN-γ in the study group was 15.61 ± 4.40 % before desensitization and 15.08 ± 5.89 % after desensitization. The rate of IFN-γ secreting CD4+ T lymphocytes was 20.51 ± 4.41 % in the normal control group and 16.07 ± 5.7 % in the ATA group (p = 0.021). The ratio of CD4+ T lymphocyte secreting IFN-γ was reduced in patients with AERD before desensitization compared to normal control group (p = 0.040). The levels of IL-2, IL-4, and the subsets of lymphocyte were not different before and after desensitization compared to control groups.

摘要

阿司匹林加重的呼吸道疾病(AERD)是由乙酰水杨酸(ASA)和/或非甾体抗炎药(NSAIDs)引起的。先前已经研究了脱敏对许多介质的影响,但很少有研究涉及脱敏对 T 淋巴细胞和 T 淋巴细胞衍生细胞因子的影响。本研究旨在检查阿司匹林敏感的哮喘患者在阿司匹林脱敏前后外周血淋巴细胞(PBL)细胞因子的表达。在这项研究中,还在细胞内水平测量了 CD4+T 淋巴细胞在阿司匹林脱敏前释放白细胞介素-2(IL-2)、白细胞介素-4(IL-4)和干扰素-γ(IFN-γ)的情况,并在 1 个月后评估了阿司匹林脱敏后这些细胞因子的表达情况。研究纳入了 12 例 AERD 患者。形成了两个不同的对照组,一组由 15 名健康人组成,另一组由 12 名使用阿司匹林的阿司匹林耐受哮喘(ATA)患者组成。在脱敏前采集了一份血样,在 4 天脱敏治疗后采集了第二份血样进行重复检测。在研究组中,脱敏前分泌 IFN-γ的淋巴细胞比例为 15.61±4.40%,脱敏后为 15.08±5.89%。在正常对照组中,分泌 IFN-γ的 CD4+T 淋巴细胞的比率为 20.51±4.41%,在 ATA 组中为 16.07±5.7%(p=0.021)。与正常对照组相比,AERD 患者脱敏前 CD4+T 淋巴细胞分泌 IFN-γ的比例降低(p=0.040)。与对照组相比,脱敏前后 IL-2、IL-4 和淋巴细胞亚群的水平无差异。

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