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The clinical and environmental determinants of airway transcriptional profiles in allergic asthma.

Publication ,  Journal Article
Yang, IV; Tomfohr, J; Singh, J; Foss, CM; Marshall, HE; Que, LG; McElvania-Tekippe, E; Florence, S; Sundy, JS; Schwartz, DA
Published in: Am J Respir Crit Care Med
March 15, 2012

RATIONALE: Gene expression profiling of airway epithelial and inflammatory cells can be used to identify genes involved in environmental asthma. METHODS: Airway epithelia and inflammatory cells were obtained via bronchial brush and bronchoalveolar lavage (BAL) from 39 subjects comprising three phenotypic groups (nonatopic nonasthmatic, atopic nonasthmatic, and atopic asthmatic) 4 hours after instillation of LPS, house dust mite antigen, and saline in three distinct subsegmental bronchi. RNA transcript levels were assessed using whole genome microarrays. MEASUREMENTS AND MAIN RESULTS: Baseline (saline exposure) differences in gene expression were related to airflow obstruction in epithelial cells (C3, ALOX5AP, CCL18, and others), and to serum IgE (innate immune genes and focal adhesion pathway) and allergic-asthmatic phenotype (complement genes, histone deacetylases, and GATA1 transcription factor) in inflammatory cells. LPS stimulation resulted in pronounced transcriptional response across all subjects in both airway epithelia and BAL cells, with strong association to nuclear factor-κB and IFN-inducible genes as well as signatures of other transcription factors (NRF2, C/EBP, and E2F1) and histone proteins. No distinct transcriptional profile to LPS was observed in the asthma and atopy phenotype. Finally, although no consistent expression changes were observed across all subjects in response to house dust mite antigen stimulation, we observed subtle differences in gene expression (e.g., GATA1 and GATA2) in BAL cells related to the asthma and atopy phenotype. CONCLUSIONS: Our results indicate that among individuals with allergic asthma, transcriptional changes in airway epithelia and inflammatory cells are influenced by phenotype as well as environmental exposures.

Duke Scholars

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Published In

Am J Respir Crit Care Med

DOI

EISSN

1535-4970

Publication Date

March 15, 2012

Volume

185

Issue

6

Start / End Page

620 / 627

Location

United States

Related Subject Headings

  • Young Adult
  • Respiratory System
  • Respiratory Mucosa
  • RNA
  • Male
  • Immunoglobulin E
  • Immunity, Innate
  • Hypersensitivity
  • Humans
  • Gene Expression
 

Citation

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Yang, I. V., Tomfohr, J., Singh, J., Foss, C. M., Marshall, H. E., Que, L. G., … Schwartz, D. A. (2012). The clinical and environmental determinants of airway transcriptional profiles in allergic asthma. Am J Respir Crit Care Med, 185(6), 620–627. https://doi.org/10.1164/rccm.201108-1503OC
Yang, Ivana V., John Tomfohr, Jaspal Singh, Catherine M. Foss, Harvey E. Marshall, Loretta G. Que, Erin McElvania-Tekippe, Sarita Florence, John S. Sundy, and David A. Schwartz. “The clinical and environmental determinants of airway transcriptional profiles in allergic asthma.Am J Respir Crit Care Med 185, no. 6 (March 15, 2012): 620–27. https://doi.org/10.1164/rccm.201108-1503OC.
Yang IV, Tomfohr J, Singh J, Foss CM, Marshall HE, Que LG, et al. The clinical and environmental determinants of airway transcriptional profiles in allergic asthma. Am J Respir Crit Care Med. 2012 Mar 15;185(6):620–7.
Yang, Ivana V., et al. “The clinical and environmental determinants of airway transcriptional profiles in allergic asthma.Am J Respir Crit Care Med, vol. 185, no. 6, Mar. 2012, pp. 620–27. Pubmed, doi:10.1164/rccm.201108-1503OC.
Yang IV, Tomfohr J, Singh J, Foss CM, Marshall HE, Que LG, McElvania-Tekippe E, Florence S, Sundy JS, Schwartz DA. The clinical and environmental determinants of airway transcriptional profiles in allergic asthma. Am J Respir Crit Care Med. 2012 Mar 15;185(6):620–627.

Published In

Am J Respir Crit Care Med

DOI

EISSN

1535-4970

Publication Date

March 15, 2012

Volume

185

Issue

6

Start / End Page

620 / 627

Location

United States

Related Subject Headings

  • Young Adult
  • Respiratory System
  • Respiratory Mucosa
  • RNA
  • Male
  • Immunoglobulin E
  • Immunity, Innate
  • Hypersensitivity
  • Humans
  • Gene Expression