FIGURE 1.

Early-life exposures, immune maturation and priming of the developing lung for disease. The prenatal and perinatal environments can have profound effects on the development and progression of respiratory diseases. Different maternal exposures (diet, smoking, medication usage) and maternal inflammation can promote fetal immune programming. Moreover, early-life colonisation of the lungs is imperative for shaping of the immune response. Early-life changes in lung development, specific environmental exposures and alterations in lung immune maturation following such changes and exposures can lead to the development of childhood and adult respiratory diseases. Alterations in what is considered “healthy” lung development, caused by, for example, chorioamnionitis-associated bronchopulmonary dysplasia (BPD), or aberrant lung structure associated with preterm birth may prime the neonate, via changes in immune maturation or cellular mechanisms in the lung, for increased susceptibility to develop respiratory complications in later life. IL: interleukin; ST: suppression of tumorigenicity; ILC: innate lymphoid cell; Th: T-helper; PH: pulmonary hypertension.