The prevalence of allergic asthma has reached epidemic proportions, especially in Westernized countries. This chronic inflammatory lung disease is caused by an exaggerated immune response to inhaled allergens such as house dust mite, pollen and animal dander. Research has shown that most patients become sensitized to allergen early in life and that several environmental factors can influence the risk for asthma development. For instance, growing up on a traditional farm has proven to reduce the risk for allergic asthma, whereas infection with respiratory syncytial virus (RSV) - a pneumovirus - in early life has shown to promote asthma development. In both cases it is thought that modifications in long-lived resident cells make persons more or less susceptible toward allergic sensitization. One such long-lived lung resident cell is the alveolar macrophage, who's role in the asthma pathogenesis is still unclear. Interestingly, it has recently been shown that macrophages can adapt their function following viral infections or exposure to endotoxins. Therefore, I want to study the role of alveolar macrophages in allergic asthma and investigate whether pneumovirus infection, farm dust and LPS can alter alveolar macrophages in such way that they contribute to the promotion or suppression of allergic asthma by these environmental factors. This project might reveal insights in how the environment affects the susceptibility for asthma development.