My laboratory studies mechanisms of inflammatory responses relevant to airway diseases characterized by inflammation and mucin overproduction, e.g., cystic fibrosis (CF), asthma, and chronic obstructive pulmonary disease (COPD). We have published key papers on the role of alterations in calcium signaling for inflammatory responses relevant to CF, and the importance of mitochondria in restricting calcium-mediated functions in polarized airway epithelia. During the last few years, we discovered that CF airway epithelial inflammation enhances the efficacy of CFTR modulators, which is a novel paradigm in the CF field. We are currently investigating the mechanisms mediating inflammation-enhanced CFTR rescue.We also study the role of the Unfolded Protein Response (UPR) in airway inflammatory responses. We were the first to implicate the UPR pathway mediated by the ubiquitous inositol requiring enzyme 1α (IRE1α) in cytokine production by human bronchial epithelia (http://www.ncbi.nlm.nih.gov/pubmed/19321437), and made the key discovery that the isoform IRE1β is only expressed in mucous cells and is required for airway epithelial mucin production (http://www.ncbi.nlm.nih.gov/pubmed/23168839). The latter discovery led to a startup company that aims to generate IRE1β inhibitors as novel therapeutics for airway muco-obstructive diseases.We are also investigating the functional role of additional branches of the UPR in other aspects of pulmonary inflammation (http://www.ncbi.nlm.nih.gov/pubmed/21030518; http://www.ncbi.nlm.nih.gov/pubmed/22697344), and in cigarette smoke-induced alterations in airway epithelial function.