CA2+, GAP JUNCTIONS & COMMUNICATION IN ALVEOLAR II CELLS

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Respiratory ailments are responsible for a significant number of general practitioner (approximately 25 percent) and hospital (approximately 30 percent) visits each year. Many of these ailments are rooting in the dysfunctional cellular physiology of alveolar type II cells. Alveolar type II cells are epithelial cells that contribute to the lining of the lung. Among other things, these cells provide critical secretions in the lung that keep the lung from collapsing and provide for a proper aqueous environment that allows for proper oxygen exchange. Just as importantly, alveolar cells are crucial in general maintenance of the cellular layer following insult or injury. Dysfunction of alveolar II cells, as seen after severe cases of asthma, chronic bronchitis, bronchiectasis, infection or injury, can have serious effects on lung physiology, (e.g. reduced O2 transfer, altered liquid interface, or misplacement of cell types at the lung surface that further exasperate the diseased state). At any given time, there are tens to hundreds of thousands of alveolar II cells working together to maintain lung homeostasis. However, there is little known concerning the cellular mechanisms that allow for alveolar cells work together for normal lung function. It is the purpose of this proposal to utilize advanced microscopy techniques that allows us to monitor communication pathways between cells and discover how alveolar cells coordinate their function. It is essential that we understand the basic cellular processes that lead to communicated and coordinated tissue and organ outcomes. With a model system for alveolar intercellular communication could expedite the formulating and testing of new medical treatments for dysfunctional alveolar cell physiology that underlies specific airway conditions following disease, insult and injury in the lung.