Deficient antiviral immune responses in childhood: Distinct roles of atopy and asthma
Deficient antiviral immune responses in childhood: Distinct roles of atopy and asthma
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DOI：
10.1016/j.jaci.2012.08.005
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发表时间：
2012-12-01
影响因子：
14.2
通讯作者：
Papi, Alberto
中科院分区：
文献类型：
--
作者：
Baraldo, Simonetta;Contoli, Marco;Papi, Alberto
背景：特应性哮喘患者对病毒感染的免疫应答受损最近被报道和争论。这种情况是否存在于儿童期以及是否受特应性本身的影响值得进一步研究。目的：我们试图研究哮喘、特应性或两者兼而有之的儿童鼻病毒感染时气道干扰素的产生及其与气道炎症的关系。方法：从47名接受支气管镜检查的儿童（平均年龄5 ± 0.5岁）中获得支气管活检标本和上皮细胞。研究人群包括特应性或非特应性哮喘儿童，无哮喘的特应性儿童，以及无特应性或哮喘的儿童。在支气管上皮细胞培养物中评估鼻病毒16型对IFN-λ和IFN-β mRNA和蛋白水平的诱导。免疫组织化学方法在支气管活检samples.Results：鼻病毒16型诱导的干扰素的生产显着减少，在特应性哮喘，非特应性哮喘，和特应性非哮喘儿童相比，在非特应性非哮喘儿童（所有P <0.05）。鼻病毒RNA水平的增加导致了干扰素诱导的缺陷。此外，IFN-1和IFN-b诱导与气道T（H）2免疫病理学特征（嗜酸性粒细胞增多和IL-4阳性：分别为P <0.05和r = -0.38和P <0.05和r =-0.58）和上皮损伤（P <0.05和r = -0.55）呈负相关。此外，血清总IgE水平与鼻病毒诱导的IFN-1 mRNA水平呈负相关（P <0.05和r = -0.41），与鼻病毒RNA水平呈正相关（P <0.05和r = 0.44）。结论：在儿童期哮喘受试者中，无论其特应性状态如何，以及在无哮喘的特应性患者中，均存在对鼻病毒感染的干扰素应答缺陷。这些发现表明，对病毒感染的免疫反应缺陷并不局限于特应性哮喘患者，也存在于其他T（H）2导向疾病的患者中。（J Allergy Clin Immunol 2012;130：1307-14.）
Background: Impaired immune response to viral infections in atopic asthmatic patients has been recently reported and debated. Whether this condition is present in childhood and whether it is affected by atopy per se deserves further investigation.Objective: We sought to investigate airway interferon production in response to rhinovirus infection in children who are asthmatic, atopic, or both and its correlation with the airway inflammatory profile.Methods: Bronchial biopsy specimens and epithelial cells were obtained from 47 children (mean age, 5 +/- 0.5 years) undergoing bronchoscopy. The study population included asthmatic children who were either atopic or nonatopic, atopic children without asthma, and children without atopy or asthma. Rhinovirus type 16 induction of IFN-lambda and IFN-beta mRNA and protein levels was assessed in bronchial epithelial cell cultures. The immunoinflammatory profile was evaluated by means of immunohistochemistry in bronchial biopsy specimens.Results: Rhinovirus type 16-induced interferon production was significantly reduced in atopic asthmatic, nonatopic asthmatic, and atopic nonasthmatic children compared with that seen in nonatopic nonasthmatic children (all P < .05). Increased rhinovirus viral RNA levels paralleled this deficient interferon induction. Additionally, IFN-l and IFN-b induction correlated inversely with the airway T(H)2 immunopathologic profile (eosinophilia and IL-4 positivity: P < .05 and r = -0.38 and P < .05 and r = -0.58, respectively) and with epithelial damage (P < .05 and r = -0.55). Furthermore, total serum IgE levels correlated negatively with rhinovirus-induced IFN-l mRNA levels (P < .05 and r = -0.41) and positively with rhinovirus viral RNA levels (P < .05 and r = 0.44).Conclusions: Deficient interferon responses to rhinovirus infection are present in childhood in asthmatic subjects irrespective of their atopic status and in atopic patients without asthma. These findings suggest that deficient immune responses to viral infections are not limited to patients with atopic asthma but are present in those with other T(H)2-oriented conditions. (J Allergy Clin Immunol 2012;130:1307-14.)