喘息婴幼儿外周血气道炎症相关介质水平的研究

目的 通过检测喘息婴幼儿外周血相关炎症介质水平，从辅助性T细胞（Th）1/Th2失衡及气道炎症两个方面探讨婴幼儿喘息发生的可能机制。方法 选取急性喘息发作婴幼儿50例为喘息组，25例健康婴幼儿为健康对照组。喘息组患儿依据喘息发生次数分为首次喘息组（首发组）25例和反复喘息组（反复组，发作次数≥ 2次）25例；根据是否存在哮喘发生的高危因素分为有高危因素组22例和无高危因素组28例；根据病原学检测结果分为病原学阳性组23例和病原学阴性组27例。检测各组外周血Th1细胞因子白介素（IL）-2，Th2细胞因子IL-4、IL-5、IL-13、转化生长因子-β1（TGF-β1），以及总IgE （TIgE）水平。喘息组患儿同时送检外周血嗜酸性粒细胞（EOS）计数，并采集标本进行呼吸道病原学检测。结果 喘息组外周血IL-4、IL-5、IL-13、TGF-β1及TIgE水平较健康对照组均明显升高（P < 0.05）；外周血IL-2、IL-4、IL-5、IL-13、TGF-β1及TIgE水平在首发组与反复组，有哮喘高危因素组与无哮喘高危因素组，以及病原学阳性组与病原学阴性组之间比较，差异均无统计学意义（P > 0.05）。相关性分析表明喘息组外周血EOS计数与IL-4水平呈正相关（P < 0.01）；IL-4水平与IL-5、IL-13水平呈正相关（P < 0.01）；IL-5水平与IL-13水平呈正相关（P < 0.01）；IL-2水平与TGF-β1水平呈正相关（P < 0.05）。结论 喘息婴幼儿存在Th1/Th2失衡，表现为Th2优势表达；IL-4、IL-5、IL-13、TGF-β1及IgE共同参与了婴幼儿喘息性疾病的发病过程。喘息婴幼儿存在气道炎症，与喘息发作次数、是否存在哮喘高危因素及病原学检测是否阳性无关。

Levels of airway inflammatory mediators in peripheral blood in infants and young children with wheezing

Objective To examine the levels of airway inflammatory mediators in peripheral blood in infants and young children with wheezing and to study the possible pathogenesis of wheezing from the aspects of T helper cell 1 (Th1)/T helper cell 2 (Th2) imbalance and airway inflammation. Methods A total of 50 children aged 1 month to 3 years with an acute wheezing episode were enrolled as the wheezing group, and 25 age-matched healthy infants were enrolled as the healthy control group. According to the number of wheezing episodes, the wheezing group was divided into a first-episode group (n=25) and a recurrent wheezing (number of episodes ≥ 2) group (n=25). According to the presence or absence of high-risk factors for asthma, the wheezing group was divided into a high-risk factor group (n=22) and a non-high-risk factor group (n=28). According to the results of pathogen detection, the wheezing group was divided into a positive pathogen group (n=23) and a negative pathogen group (n=27). Levels of interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13), transforming growth factor-β1 (TGF-β1), and total IgE (TIgE) in peripheral blood were measured for each group. For children with wheezing, eosinophil (EOS) count in peripheral blood was measured, and related samples were collected for respiratory pathogen detection. Results The wheezing group had significantly higher levels of IL-4, IL-5, IL-13, TGF-β1, and TIgE in peripheral blood than the healthy control group (P < 0.05). There were no significant differences in the levels of IL-2, IL-4, IL-5, IL-13, TGF-β1, and TIgE in peripheral blood between the first-episode and recurrent wheezing groups, between the high-risk factor and non-high-risk factor groups, and between the positive pathogen and negative pathogen groups (P > 0.05). The correlation analysis showed that in children with wheezing, EOS count was positively correlated with IL-4 level (P < 0.01), IL-4 level was positively correlated with IL-5 and IL-13 levels (P < 0.01), IL-5 level was positively correlated with IL-13 level (P < 0.01), and IL-2 level was positively correlated with TGF-β1 level (P < 0.05). Conclusions Th1/Th2 imbalance with a predominance of Th2 is observed in infants and young children with wheezing. IL-4, IL-5, IL-13, TGF-β1, and IgE are involved in the pathogenesis of wheezing in these children. Airway inflammation is also observed in these children with wheezing, but it is not associated with the number of wheezing episodes, presence or absence of high-risk factors for asthma, or results of pathogen detection.