Evaluation of airway reactivity and immune characteristics as risk factors for wheezing early in life.

Evaluation of airway reactivity and immune characteristics as risk factors for wheezing early in life.
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DOI:
10.1016/j.jaci.2010.06.028
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发表时间:
2010-09
影响因子:
14.2
通讯作者:
Tepper, Robert S.
Tepper, Robert S.
中科院分区:
医学1区
文献类型:
--
作者:
Yao, Weiguo;Barbe-Tuana, Florencia M.;Llapur, Conrado J.;Jones, Marcus H.;Tiller, Christina;Kimmel, Risa;Kisling, Jeffrey;Nguyen, Evelyn T.;Nguyen, James;Yu, Zhangsheng;Kaplan, Mark H.;Tepper, Robert S.

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儿童哮喘最常见的特征是反复喘息、气道高反应性和特应性;然而,我们对生命早期这些关系的理解仍不清楚。生命早期的呼吸道疾病和特应性致敏可能会产生先天性和获得性免疫反应之间的相互作用,导致气道炎症和气道反应性升高。我们假设,在1年的随访中,没有喘息发作的婴儿发病前的气道反应性和免疫学特征与随后的喘息有关。116名患有慢性皮炎的婴儿在喘息发作前入组。气道反应性,过敏原特异性IgE,刺激外周血单核细胞(PBMC)的细胞因子的产生,和树突状细胞的百分比进行了测量后进入和气道反应性进行了重新评估,在1年的随访。线性回归模型用于评估预测因素对连续结局的影响。牛奶和/或鸡蛋致敏与喘息发作前和喘息发作后气道反应性升高相关;然而,这些因素与喘息风险增加无关。初始气道反应性和喘息作为随访时气道反应性的决定因素之间存在相互作用。此外,刺激PBMC产生的细胞因子是喘息的危险因素,而增加常规树突状细胞的百分比对喘息具有保护作用。我们在一个选定的婴儿队列中的数据支持了一个模型,该模型具有与初始气道反应性无关的随后喘息的多个危险因素;然而,在生命早期产生喘息的病因学因素可能有助于气道反应性升高。
Childhood asthma is most often characterized by recurrent wheezing, airway hyper-reactivity, and atopy; however, our understanding of these relationships from early in life remains unclear. Respiratory illnesses and atopic sensitization early in life may produce an interaction between innate and acquired immune responses leading to airway inflammation and heightened airway reactivity. We hypothesized that pre-morbid airway reactivity and immunologic characteristics of infants without prior episodes of wheezing would be associated with subsequent wheezing during 1-year follow-up. 116 infants with chronic dermatitis were enrolled prior to episodes of wheezing. Airway reactivity, allergen-specific IgE, cytokine production by stimulated peripheral blood mononuclear cells (PBMCs), and percentages of dendritic cells were measured upon entry and airway reactivity was reassessed at 1-year follow-up. Linear regression models were used to evaluate predictor’s effect on continuous outcomes. milk and/or egg sensitization was associated with heightened airway reactivity prior to wheezing and after the onset of wheezing; however, these factors were not associated with an increased risk of wheezing. There was an interaction between initial airway reactivity and wheezing as a determinant of airway reactivity at follow-up. In addition, cytokine production by stimulated PBMCs was a risk factor for wheezing, while increased percentages of conventional dendritic cells were protective for wheezing. Our data in a selected cohort of infants support a model with multiple risk factors for subsequent wheezing that are independent of initial airway reactivity; however, the etiologic factors that produce wheezing very early in life may contribute to heightened airway reactivity.
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