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Pulmonary Innate Lymphoid Cells and airway inflammation in C

Institution: University of California, Davis
Investigator(s): Angela Haczku, M.D., Ph.D.
Award Cycle: 2018 (Cycle 27) Grant #: 27IR-0053 Award: $937,500
Subject Area: Pulmonary Disease
Award Type: High Impact Research Project Award
Abstracts

Initial Award Abstract

Chronic cigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD), the third leading cause of death globally. There is no effective treatment for COPD. Acute flare ups of the disease, called exacerbations, may lead to worsening of symptoms and even hospitalization. These exacerbations reduce quality of life and are a huge economic burden for COPD patients. Exacerbations are characterized by the influx of inflammatory cells from the peripheral blood to the airways induced by exposure to infections or environmental factors such as the toxic air pollutant, ozone. Studies investigating the mechanisms of ozone-induced COPD exacerbations are few, and thus how ozone impacts COPD patients is largely unknown. In our project we will address why COPD patients are more susceptible to air pollutant-induced exacerbations. To understand this phenomenon, we will study (1) an immuno-protective protein called Surfactant Protein-D (SP-D) released into the airways in order to suppress inflammation caused by ozone inhalation, and (2) an immune cell type (ILC2) that causes inflammation in the lung after ozone exposure. We will answer the questions how SP-D interacts with and alters the function of ILC2 in healthy individuals and in those with COPD, and how ILC2 elicits airway inflammation after ozone inhalation. Upon successful completion, this work will increase our understanding of how air pollutants lead to COPD exacerbations with the identification of potentially novel therapeutic targets to treat this devastating disease.