Allergy Department, 2nd Pediatric Clinic, National and Kapodistrian University of Athens, Athens, Greece.
Division of Infection, Immunity and Respiratory Medicine, University of Manchester, Manchester, UK.
Pediatr Allergy Immunol. 2024 Mar;35(3):e14098. doi: 10.1111/pai.14098.
Wheezing is the cardinal symptom of asthma; its presence early in life, mostly caused by viral infections, is a major risk factor for the establishment of persistent or recurrent disease. Early-life wheezing and asthma exacerbations are triggered by common respiratory viruses, mainly rhinoviruses (RV), and to a lesser extent, respiratory syncytial virus, parainfluenza, human metapneumovirus, coronaviruses, adenoviruses, influenza, and bocavirus. The excess presence of bacteria, several of which are part of the microbiome, has also been identified in association with wheezing and acute asthma exacerbations, including haemophilus influenza, streptococcus pneumoniae, moraxella catarrhalis, mycoplasma pneumoniae, and chlamydophila pneumonia. While it is not clear when asthma starts, its characteristics develop over time. Airway remodeling already appears between the ages of 1 and 3 years of age even prior to the presence of atopic inflammation or an asthma diagnosis. The role of genetic defect or variations hampering the airway epithelium in response to environmental stimuli and severe disease morbidity are now considered as major determinants for early structural changes. Repeated viral infections can induce and perpetuate airway hyperresponsiveness. Allergic sensitization, that often precedes infection-induced wheezing, shifts inflammation toward type-2, while common respiratory infections themselves promote type-2 inflammation. Nevertheless, most children who wheeze with viral infections during infancy and during preschool years do not develop persistent asthma. Multiple factors, including illness severity, viral etiology, allergic sensitization, and the exposome, are associated with disease persistence. Here, we summarize current knowledge and developments in infection epidemiology of asthma in children, describing the known impact of each individual agent and mechanisms of transition from recurrent wheeze to asthma.
喘息是哮喘的主要症状；其在生命早期出现，主要由病毒感染引起，是持续性或复发性疾病发生的主要危险因素。生命早期的喘息和哮喘加重是由常见的呼吸道病毒引起的，主要是鼻病毒（RV），其次是呼吸道合胞病毒、副流感病毒、人偏肺病毒、冠状病毒、腺病毒、流感病毒和博卡病毒。细菌的过度存在，其中有几种是微生物组的一部分，也与喘息和急性哮喘加重有关，包括流感嗜血杆菌、肺炎链球菌、卡他莫拉菌、肺炎支原体和肺炎衣原体。虽然目前还不清楚哮喘何时开始，但它的特征会随着时间的推移而发展。气道重塑甚至在特应性炎症或哮喘诊断之前，在 1 至 3 岁之间就已经出现。遗传缺陷或阻碍气道上皮对环境刺激和严重疾病发病率做出反应的变异的作用，现在被认为是早期结构变化的主要决定因素。反复的病毒感染可诱发和持续气道高反应性。过敏致敏通常先于感染引起的喘息，将炎症转向 2 型，而常见的呼吸道感染本身则促进 2 型炎症。然而，大多数在婴儿期和学龄前因病毒感染而喘息的儿童不会发展为持续性哮喘。多种因素，包括疾病严重程度、病毒病因、过敏致敏和外显子组，与疾病的持续存在有关。在这里，我们总结了儿童哮喘感染流行病学的现有知识和进展，描述了每个单独的病原体的已知影响以及从反复喘息向哮喘转变的机制。
