Grant: Operating Grant

The inflammatory response is essential for survival. Indeed, the accuracy and effectiveness of the immune system is key in multiple protective reactions such as clearing of infections and repairing of injuries, particularly in areas which are in direct contact with possible pathogens such as the lung. However, the control of the intensity and duration of the inflammatory response is equally important in maintaining homeostasis. A loss of control of this defence mechanism can lead to irreparable wounding and alterations in lung function. In the case of many inflammatory lung diseases such as asthma, the intensity and chronicity of the inflammation is responsible for most symptoms. The mechanisms regulating the inflammatory response as well as the steps leading to chronic lung inflammation have been the subject of the majority of basic research in the field of inflammation. Although these studies opened many therapeutic avenues, most current therapies aim at blocking the inflammatory response which can cause a variety of undesirable side effects and resistance, strengthening the need for new therapeutic strategies. We believe that therapies targeting molecules participating in the control of the lung inflammatory response, in the attempt to restore homeostasis would possess a considerable advantage over traditional and current therapies. However, the exact mechanisms under which the control of the pulmonary inflammatory response is regulated are poorly understood. Recently, our laboratory has made the striking observation that mice lacking the alpha-E integrin CD103 develop worse asthma. Therefore, using mouse models of asthma, genetically modified mice and in vitro studies, we focus on better understanding the role of this specific moelcule in the developement of airway inflammation, in the hope of shedding a light on this mechanism as a possible interesting new therapeutic avenue.