Asthma is the most prevalent childhood chronic condition. In opposition to adult asthma, asthma occurring in children usually is distinguished by a personalised and sometimes family history of atopy and associated inflammatory markers of type 2. Family and personal records of atopic diseases are confirmed as significant asthma and infant persistence risk factors. In early childhood and with various sensitivities to aeroallergens, the risk of asthma occurrence in school years is greatly increased. Early life lower respiratory tubes, especially rhinoviral infections often increase the sensitivity of children to atopic asthma. CDHR3 polymorphism of rhinoviruses Type C receptors has been found to affect the expression, activation and progression of asthma and the degree of exacerbation in infants. The suspective asthma can be synergistically enhanced by various pathways of atopic sensitization and respiratory viral infections, including by suppression of endogenous antiviral responses to rhinoviruses.
Emerging causes, including the susceptibility of early childhood to environmental factors and the structure of the Lung and gut Microbiomes, often include asthma pathogenesis in genetically predisposed people.
In the present study, new research issues including epigenetic and pulmonary microbiome are outlined on the difficult role played by the atopy in asthma pathogenesis and persistence.
