Role of Epigenetics in the Pathogenesis, Treatment, Prediction, and Cellular Transformation of Asthma

Figure 3

The two peaks of human asthma and the role of epigenetics in the cellular transformation of childhood asthma to adult-onset/old age asthma. (a) The two peaks of human asthma are childhood asthma (↑ IgE, ↑ eosinophils, FeNO, corticosteroid sensitive, and T2 high) and adult-onset/old age asthma (neutrophilic/paucigranulocytic, corticosteroid less sensitive, and non-T2 asthma) with airway smooth muscle or neural dysfunction, possible association with comorbidities [5, 6], and periods of remission in some cases. However, we should not forget that these profiles are not strictly age-limited (children and adults may have eosinophilic, neutrophilic, or even paucigranulocytic asthma with overlapping steroid response), and several other components of the immune, neuronal, and hormonal responses are also involved with asthma. (b) The two peaks of asthma (childhood asthma and adulthood as adult-onset/old age asthma). In general, there is male dominance in childhood asthma, with a shift to female dominance in later peak. Components of epigenetic mechanisms, as well as cells involved in asthma, are also shown, as their interaction is needed in asthma epigenetics. The long arrows in (a) show the possible point of commencement and involvement of epigenetic mechanisms, as we believe, in the cellular transformation of childhood asthma to adult-onset/old age asthma, although further epigenetic research is required in the future. IgE: immunoglobulin E; miRNAs: micro-RNAs; FeNO: fractional exhaled nitric oxide.

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