Although the prevalence of inflammatory airway diseases is steadily growing, our knowledge regarding the underlying molecular and cellular mechanisms is fragmentary. The striking simplicity of the fruit fly's airway epithelium, which is composed of epithelial cells only, justifies its use as a model to study general features and response characteristics of airway epithelia in general. Infection with the gram-negative pathogen Erwinia carotovora induces an immune response in all epithelial cells via activation of the immune deficiency (IMD) pathway, but the transcriptional profile differs significantly from that observed after ectopic activation of this signaling pathway. After strong infections, genes controlling central aspects of tracheal development are reactivated, a response that is not seen after ectopic IMD pathway activation. Presumably to counteract infection-induced cell death-promoting signals, a survival response is launched, characterized by the concurrent expression and activation of the longevity genes dfoxo and dthor. Regions of the airways featuring the strongest immune reactions show substantial remodeling, which is characterized by a significant thickening of the epithelial cells. In conclusion, features related to those observed in inflammatory diseases of the human airways are apparently part of the normal response repertoire of airway epithelia to infection.