 Asthma has a large impact on the children of our society. It is among the most common chronic diseases of childhood and is the leading cause of absenteeism from school. It is unknown as to why more children are having recurrent episodes of wheezing and why some children have asthma while others do not. There is increasing evidence that differences in innate immune responses among children can determine which child will have recurrent wheezing and asthma. While many studies have focused on the factors that initiate innate immune responses, there are relatively few studies of the downstream factors that cause abnormal airway responses. There is evidence that eicosanoid mediators are part of the innate immune response and can function as its effector arm for allergic responses. The ability of leukotrienes and prostaglandins to produce central features of the asthma phenotype is well described and there is emerging evidence that lipoxins facilitate restoration of allergic changes in the airways. This study will test the hypothesis that the balance of airway eicosanoid expression during early-life wheezing illness and the genetically determined capacity to respond will predict recurrent wheezing. Moreover, an intervention to restore a more normal tissue response to this imbalance will reduce symptoms of early-life wheezing and subsequent recurrent episodes. 