BYU

Abstract by James Woods

Personal Infomation


Presenter's Name

James Woods

Degree Level

Undergraduate

Co-Authors

Jonard Valdoz
Connor Knight
Alejandro Zegarra

Abstract Infomation


Department

Chemistry and Biochemistry

Faculty Advisor

Pam Van Ry

Title

The Role of Gastroesophageal Reflux in Idiopathic Pulmonary Fibrosis

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is an incurable and terminal lung disease of unknown cause. Around 90% of IPF patients have a comorbidity of gastroesophageal reflux disease (GERD). To determine whether GERD is a cause of IPF, we utilized A549, HEK293T, and HEPG2 epithelial cells to model the disease induction through acid and pepsin exposures--two major components of gastric acid. Treatments were varied to include pulsed (<24 hr), short-term (<7 day) and long-term multi-passage treatments to simulate chronic GER. Emphasis was placed on markers for epithelial-mesenchymal transition (EMT) a process that has been implicated in fibrosis. Our data show that TGF-Beta signaling is elevated in a serum dependent manner when cells are exposed to acid.The addition of active pepsin did not have an additive effect on stimulation of the TGF-Beta pathway but seemed to have an additive effect on EMT markers when treatment was extended. Our chronic exposure experiments also showed significant EMT. Together these data suggest that acidification and peptic activity may cause lung fibrosis through EMT of the lung epithelium.