Early life origins of asthma

It is increasingly clear that the seeds of the asthmatic diathesis are planted early in life, possibly in utero. The cellular and molecular events that are responsible for these important disease processes are only now being identified. Genetic factors play a crucial role. In addition, the in utero microenvironment and neonatal immune system are now appreciated to be intrinsically skewed toward a Th2 (rather than Th1) immune response. When the genetically predisposed individual then encounters key environmental factors, an immune/inflammatory response ensues that ultimately directs the development of allergic disease and, through processes not fully defined, focuses these immune-regulated inflammatory responses into the lower airway (Figure ​(Figure22). Figure 2 The early life origins can be divided into a number of phases. Early life events can lead to the development of a Th2-like environment, which is influenced by infections (Th1) rather than allergen exposure, diet, and certain respiratory infections. The ... A variety of levels of investigation suggest that there are crucial temporal windows in babies and children during which these important patient-environment interactions need to occur for full disease expression, and that a variety of agents, including respiratory infections, diet, and toxin exposure, can all interact to regulate the final phenotype. The culmination of these multiple events is the development of Th2-like inflammation, bronchial hyperresponsiveness, and air flow obstruction/clinical asthma. The appreciation that these events begin early in life has refined our thought processes regarding disease pathogenesis, and has provided new experimental targets for investigators. Hopefully, an enhanced understanding of the pathogenesis of childhood asthma will provide the types of insights that will allow us to think in terms of primary disease prevention rather than the present goal of secondary symptom amelioration.