Perinatal Programming of Childhood Asthma

Prevalence of childhood asthma has worldwide increased in recent decades. Different genome-wide studies have identified that more than 100 genes in 22 chromosomes were associated with asthma. Different genetic backgrounds in different environments might modulate the susceptibility of asthma. This has been attributed to industrialized environment such as air pollution andmicrobial-deprivation ecology that polarize the immune response towards allergy sensitization in perinatal stage. Recently, evidence has shown that allergy sensitizationmay occur in fetal life, and influence of fetal environment may cause epigenetic programming of diseases in adults. Apparently, asthma is not an exception from the Developmental Origins of Health and Diseases (DOHaD), in which both the preand postnatal environments could shape the developmental programming of asthma developed in infancy, childhood, and even adulthood. The association between prenatal environment and disease risk in adults is first demonstrated by Barker showing low birth weight was linked to ischemic heart disease in adult life in 1986 [1], and collaborating with Hales to raise the thrifty phenotype hypothesis emphasizing the importance of developmental plasticity in type 2 diabetes mellitus in 1992 [2]. They also proved that obesity in adults could be traced back to prenatal exposure to famine in the Dutch hunger winter of War World II [3]. Now the prenatal programming of diseases in adults have been linked to a number of chronic diseases including metabolic syndrome, type 2 diabetes, hypertension, cardiovascular disease, schizophrenia, osteoporosis, overweight/obesity, and asthma. Taken together, this suggests that childhood asthma, although heritable, is significantly affected by different environments in perinatal stage.