Factors and Pathways that Regulate CC16 in the Lungs

Abstract

Respiratory diseases are a leading cause of death worldwide, with both chronic and acute respiratory diseases causing millions of deaths each year. The progression of many respiratory diseases, such as asthma, COPD, and ARDS involves a deterioration in lung function. Currently, there are few effective treatments available to ease lung pathology caused by or associated with these respiratory diseases. Low serum concentrations of the lung protein CC16 (or club cell secretory protein) has been investigated as a potential biomarker indicative of lung function decline in patients with respiratory diseases, including asthma and COPD. CC16 is thought to play a major role in anti-inflammatory and anti-oxidative lung functions, though mechanisms through which these occur mechanistically remain somewhat elusive. In this thesis, I will review the interactions of CC16 with known receptors and binding partners and reported mechanistic pathways through which CC16-receptor interactions impact lung health and disease. In conjunction with receptors and pathways, I will also review literature regarding endogenous and exogenous factors that influence CC16 expression, whether by regulating gene expression or secretion into the lung lumen. Tying this all together, in conclusion, I will propose possible converging pathways through which CC16 expression is impacted in a variety of respiratory conditions. The knowledge gained from this review will set the stage for a greater understanding of targets and pathways that influence CC16 levels and may lead to treatments focused on increasing CC16 and easing lung pathology.