Purpose of review: Asthma is essentially a developmental disease, in which the normal growth and development of the respiratory and immune systems are affected by environmental exposures acting on underlying genetic predispositions. The purpose of this review is to examine the role of innate immunity in the lungs in the development of allergy and asthma.
Recent findings: Both the innate and adaptive arms of the immune system are immature at birth and undergo prolonged periods of postnatal maturation. As such, they are vulnerable to adverse environmental exposures, both before and after birth. Both genetic predispositions and environmentally induced epigenetic changes in gene expression are likely to contribute to the risk of asthma; however, the relative contributions are unclear. Increasing interest is focused on deficient innate responses of the respiratory epithelium to viral infections and how these may increase the risk of asthma. However, definitive proof that these are primary and not secondary effects is lacking. Although most research has concentrated on the role of respiratory viral infections in increasing the asthma risk, the recent suggestion that the lung has a resident bacteriome and potentially important viral-bacterial interactions in the lungs broadens research scope in this area.
Summary: Classic risk factors for asthma include a family history of asthma and allergies, early and persistent allergic sensitization and viral lower-respiratory infections in early life. However, these factors do not fully explain the risk. Perhaps, the resident pulmonary microbiome and the immune response that this generates during respiratory viral infections will provide the 'missing link' in the epidemiology.