The Role of Apoptosis in Alveolar Type II and Pulmonary Microvascular Endothelial Cells in the Inflammatory Response After Blunt Chest Trauma

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Severe blunt chest trauma significantly alters the local and systemic immune response. In contused lungs, recruitment of polymorphonuclear neutrophils and activation of alveolar macrophages in concert with the cytokine/chemokine network result in an inflammatory local response. Alveolar Type II cells, which are known to play an important role in immune regulatory processes after lung injury, are immune modulated by direct cellular contact or released inflammatory mediators. Since Alveolar Type II cells control surfactant production and regeneration of the epithelial part of the blood-gas barrier via regulation of apoptosis, they are involved in the development of pulmonary edema, atelectasis and hypoxemia as seen in acute respiratory distress syndrome (ARDS). Another important cell population in this respect is the pulmonary microvascular endothelium as its interaction with neutrophils and circulating mediators is crucial for posttraumatic lung inflammation. Apoptosis of pulmonary endothelial cells and Alveolar Type II cells is a pivotal mechanism in this inflammatory process. Therefore, the project aims to elucidate the initiators and pathways of apoptosis in these two cell types during the local inflammatory response after bilateral lung contusion. For these experiments, a highly reproducible rodent model of blunt chest trauma is used to induce severe pulmonary tissue trauma.