Department of Cardiac, Thoracic and Vascular Sciences, Section of Respiratory Diseases, University of Padova, Padua, Italy.
J Allergy Clin Immunol. 2012 Dec;130(6):1307-14. doi: 10.1016/j.jaci.2012.08.005. Epub 2012 Sep 13.
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.
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.
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-λ and IFN-β mRNA and protein levels was assessed in bronchial epithelial cell cultures. The immunoinflammatory profile was evaluated by means of immunohistochemistry in bronchial biopsy specimens.
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-λ and IFN-β 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-λ mRNA levels (P < .05 and r = -0.41) and positively with rhinovirus viral RNA levels (P < .05 and r = 0.44).
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.
最近有报道称，特应性哮喘患者对病毒感染的免疫反应受损，并对此进行了争论。这种情况是否存在于儿童期，以及它是否受特应性本身的影响，都需要进一步研究。
我们旨在研究儿童哮喘、特应性或两者兼有的患者对鼻病毒感染的气道干扰素产生情况，及其与气道炎症特征的相关性。
对 47 名（平均年龄 5 ± 0.5 岁）接受支气管镜检查的儿童进行支气管活检和上皮细胞采集。研究人群包括特应性哮喘儿童、非特应性哮喘儿童、非特应性无哮喘儿童和非特应性无哮喘儿童。通过鼻病毒 16 诱导支气管上皮细胞培养物中 IFN-λ和 IFN-βmRNA 和蛋白水平来评估干扰素产生情况。通过免疫组化评估支气管活检标本中的免疫炎症特征。
与非特应性非哮喘儿童相比，特应性哮喘儿童、非特应性哮喘儿童和特应性非哮喘儿童的鼻病毒 16 诱导干扰素产生显著减少（均 P <.05）。增加的鼻病毒 RNA 水平与这种干扰素诱导不足相平行。此外，IFN-λ和 IFN-β的诱导与气道 T(H)2 免疫病理特征（嗜酸性粒细胞和 IL-4 阳性：P <.05 和 r = -0.38，P <.05 和 r = -0.58）和上皮损伤（P <.05 和 r = -0.55）呈负相关。此外，总血清 IgE 水平与鼻病毒诱导的 IFN-λ mRNA 水平呈负相关（P <.05 和 r = -0.41），与鼻病毒 RNA 水平呈正相关（P <.05 和 r = 0.44）。
特应性哮喘儿童无论特应性状态如何，以及非特应性哮喘患者，对鼻病毒感染的干扰素反应均受损。这些发现表明，对病毒感染的免疫反应不足不仅限于特应性哮喘患者，也存在于其他 T(H)2 定向疾病患者中。
