Bronchial epithelial gene expression and interstitial lung abnormalities

Aravind A. Menon, Minyi Lee, Xu Ke, Rachel K. Putman, Takuya Hino, Jonathan A. Rose, Fenghai Duan, Samuel Y. Ash, Michael H. Cho, George T. O’Connor, Josée Dupuis, Hiroto Hatabu, Marc E. Lenburg, Ehab S. Billatos, Gary M. Hunninghake*, Avi Spira, Elizabeth Moses, Jennifer Beane, Josh Campbell, Jack CunninghamGang Liu, Hanqiao Liu, Sherry Zhang, Jiarui Zhang, Xingyi Shi, Carter Merenstein, Yue Zhao, Denise Aberle, Mitchell Schnall, Charles Apgar, Irene Mahon, Lindsey Dymond, Joe Bauza, Sarah Gevo, Constantine Gastonis, Helga Marquez, David Elashoff, Ignacio Wistuba, Humam Kadara, Junya Fujimoto, Clifton Dalgard, Matthew Wilkerson, Denise Aberle, George Washko, Charles M. Kinsey, Denise Fine, Ron Goldstein, Kathleen LaCerda, John Battaile, Mitchell Kroll, Bob Keith, Mary Jackson, Steve Dubinett, Gina Lee, Babak Aryanfar, Rafael Corona, Anil Vachani, Sam Soloman, Charles Atwood, Gregory Owens, Hanna Edvardsson, Pierre Massion, Trey Helton, Mary Reid, Chris Kuzniewski, Jacob Carmichael, Holly LaPerriere, J. ScottParrish, Lindsey White, Anna Kaur, Robert Browning, Maggie Nelissery, Folashade Akanni, Luis Rojas

*Corresponding author for this work

Research output: Contribution to journalLetterpeer-review


Introduction: Interstitial lung abnormalities (ILA) often represent early fibrotic changes that can portend a progressive fibrotic phenotype. In particular, the fibrotic subtype of ILA is associated with increased mortality and rapid decline in lung function. Understanding the differential gene expression that occurs in the lungs of participants with fibrotic ILA may provide insight into development of a useful biomarker for early detection and therapeutic targets for progressive pulmonary fibrosis. Methods: Measures of ILA and gene expression data were available in 213 participants in the Detection of Early Lung Cancer Among Military Personnel (DECAMP1 and DECAMP2) cohorts. ILA was defined using Fleischner Society guidelines and determined by sequential reading of computed tomography (CT) scans. Primary analysis focused on comparing gene expression in ILA with usual interstitial pneumonia (UIP) pattern with those with no ILA. Results: ILA was present in 51 (24%) participants, of which 16 (7%) were subtyped as ILA with a UIP pattern. One gene, pro platelet basic protein (PPBP) and seventeen pathways (e.g. TNF-α signalling) were significantly differentially expressed between those with a probable or definite UIP pattern of ILA compared to those without ILA. 16 of these 17 pathways, but no individual gene, met significance when comparing those with ILA to those without ILA. Conclusion: Our study demonstrates that abnormal inflammatory processes are apparent in the bronchial airway gene expression profiles of smokers with and without lung cancer with ILA. Future studies with larger and more diverse populations will be needed to confirm these findings.

Original languageEnglish
Article number245
JournalRespiratory Research
Issue number1
StatePublished - Dec 2023


  • Gene expression
  • ILA
  • Interstitial lung abnormalities
  • Interstitial lung disease
  • Lung fibrosis


Dive into the research topics of 'Bronchial epithelial gene expression and interstitial lung abnormalities'. Together they form a unique fingerprint.

Cite this