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首页> 外文期刊>The Internet Journal of Asthma, Allergy and Immunology >Serum Interleukin-13 Levels Are Elevated In Mild And Moderate Persistent Asthma
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Serum Interleukin-13 Levels Are Elevated In Mild And Moderate Persistent Asthma

机译：轻度和中度持续性哮喘患者血清白细胞介素13水平升高

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Background: Interleukin-13 is thought to play a key role in modulating airway inflammation in asthma. Elevated levels of serum interleukin-13 (IL-13) have been documented in acute severe asthma. However, there are no reports of serum IL-13 levels in mild and moderate asthmatics who form the majority of patients. Methods: In a cross sectional survey, fifty-four asthmatics and 54 age and sex matched controls were recruited prospectively from an outpatient department. Information on asthma severity and use of inhaled steroids was gathered by a questionnaire. Results: There were 32 atopic and 22 non-atopic mild-to-moderate asthmatics. The median serum IL-13 level in the whole group of asthmatics (6.67 pg/ml) was significantly higher than in normal controls (3.09 pg/ml) (p=0.001). The median serum IL-13 levels in moderate persistent asthmatics (7.72 pg/ml) and mild persistent asthmatics (5.11pg/ml) were significantly higher than in normal controls (p<0.01and p=0.03). Whereas there was a tendency for serum IL-13 levels among moderate persistent asthmatics (7.72pg/ml) to be higher than in mild persistent (5.11 pg/ml) asthmatics, the difference was not statistically significant (p=0.9). The median serum IL-13 levels were not different among patients using regular inhaled glucocorticoids (6.72 pg/ml) and those using only an inhaled beta-2 agonist (3.36pg/ml) (p=0.8). Conclusion: Serum IL-13 levels are elevated in mild and moderate persistent atopic and non-atopic asthmatics. These data suggest the presence of a systemic Th2 inflammatory response even in mild and moderate asthmatics, which is not abrogated by inhaled glucocorticoids. Introduction Asthma is a common respiratory disorder worldwide and the vast majority of patients exhibit mild to moderate states of clinical severity (1). IL-13 has been recognized as a key cytokine mediating allergic airway inflammation and airway remodeling in asthma which is characterized by mucous hypersecretion, airway hyper-responsiveness and sub-epithelial fibrosis (2,3). IL-13 is an immunoregulatory cytokine generated predominately by activated TH2 cells and it shares many functional properties with IL-4 (4). Animal studies have shown that the administration of either IL-13 or IL-4 confers an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha chain-dependent pathway (5). Lung fibroblasts activated by IL-4 and IL-13, may act as effector cells not only in the pathogenesis of asthma but also in lung remodeling processes (6). The role of mast cells in the expression and modulation of airways inflammation through IL-13 transcription has been highlighted by Masuda et. al. (7). Also, Brightling and associates demonstrated that in asthmatics, IL-4+ and IL-13+ cells present within the airway smooth muscle were predominantly expressed by mast cells, suggesting that IL-4 and IL-13 may play an important role in mast cell-airway smooth muscle interactions (8). Lee and associates have demonstrated elevated serum IL-13 levels in patients with acute severe asthma (9). Recently, we reported that levels of circulating serum interleukin-5, a Th-2 cytokine, were elevated in patients with mild and moderate persistent asthma(10).The genes encoding the cytokines IL-4, IL-5, IL-13, and GM-CSF are located in close proximity on human chromosome 5 and a motif in the promoters of these genes with a common palindromic sequence has been described(11). Therefore, increased expression IL-5 in asthmatics is likely to activate overproduction of IL-13 by sensitized CD4 T cells. To this effect, Jenmalm and associates have documented an increased expression of IL-4, IL-5, IL-9 and IL-13 by peripheral blood mononuclear cells (PBMC's) isolated from sensitized children after stimulation with the specific allergens(12). Therefore, it is possible that serum IL-13 levels, also a cytokine derived from Th2 cells, may be elevated in this cohort of patients with mild to moderate persistent asthma. To test this
机译：背景：白介素13被认为在调节哮喘气道炎症中起关键作用。急性重症哮喘患者血清白细胞介素13（IL-13）水平升高。然而，尚无关于构成大多数患者的轻度和中度哮喘患者血清IL-13水平的报道。方法：在一项横断面调查中，前瞻性地从门诊部招募了54名哮喘病患者和54名年龄和性别相匹配的对照组。通过问卷收集有关哮喘严重程度和吸入类固醇使用情况的信息。结果：共32例特应性哮喘和22例非特应性轻度至中度哮喘患者。整组哮喘患者的平均血清IL-13水平（6.67 pg / ml）显着高于正常对照组（3.09 pg / ml）（p = 0.001）。中度持续性哮喘患者（7.72 pg / ml）和轻度持续性哮喘患者（5.11pg / ml）的血清IL-13中位数显着高于正常对照组（p <0.01和p = 0.03）。中度持续性哮喘患者（7.72pg / ml）的血清IL-13水平高于轻度持续性哮喘（5.11 pg / ml）的趋势，但差异无统计学意义（p = 0.9）。在使用常规吸入糖皮质激素（6.72 pg / ml）的患者和仅使用吸入β-2激动剂（3.36pg / ml）的患者中，血清IL-13的中位水平没有差异（p = 0.8）。结论：轻度和中度持续性特应性和非特应性哮喘患者血清IL-13水平升高。这些数据表明，即使在轻度和中度哮喘中也存在全身性Th2炎症反应，吸入性糖皮质激素并不能消除这种反应。简介哮喘是世界范围内常见的呼吸系统疾病，绝大多数患者表现出轻度至中度的临床严重程度（1）。 IL-13被公认为是哮喘中介导过敏性气道炎症和气道重塑的关键细胞因子，其特征在于粘液分泌过多，气道高反应性和上皮下纤维化（2,3）。 IL-13是一种主要由活化的TH2细胞产生的免疫调节细胞因子，与IL-4具有许多功能特性（4）。动物研究表明，通过IL-4受体α链依赖性途径，对未免疫的T细胞缺陷型小鼠给予IL-13或IL-4可赋予哮喘样表型（5）。被IL-4和IL-13激活的肺成纤维细胞不仅可以在哮喘的发病机理中而且在肺重塑过程中起效应细胞的作用（6）。 Masuda等人已经强调了肥大细胞在通过IL-13转录表达和调节气道炎症中的作用。等（7）。此外，Brightling及其同事证明，在哮喘患者中，气道平滑肌内存在的IL-4 +和IL-13 +细胞主要由肥大细胞表达，提示IL-4和IL-13可能在肥大细胞中起重要作用。 -气道平滑肌相互作用（8）。 Lee及其同事已证明急性重症哮喘患者血清IL-13水平升高（9）。最近，我们报道了轻度和中度持续性哮喘患者的循环血清白细胞介素5（Th-2细胞因子）水平升高（10）。编码细胞因子IL-4，IL-5，IL-13， GM-CSF和GM-CSF位于人类5号染色体上，并且已经描述了这些基因的启动子中具有共同回文序列的基序（11）。因此，哮喘患者中IL-5表达的增加可能会激活致敏的CD4 T细胞过高的IL-13产生。为此，Jenmalm及其同事记录了从特定过敏原刺激后从致敏儿童中分离出来的外周血单个核细胞（PBMC）可以增加IL-4，IL-5，IL-9和IL-13的表达（12）。因此，在这个轻度至中度持续性哮喘患者队列中，血清IL-13水平（也可能是Th2细胞衍生的细胞因子）可能升高。为了测试

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