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.
中科院分区:
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.
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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