Analysis of human bronchial epithelial cell proinflammatory response to Burkholderia cenocepacia infection: Inability to secrete IL-1 β

Devyn D. Gillette, Prexy A. Shah, Thomas Cremer, Mikhail A. Gavrilin, Beth Y. Besecker, Anasuya Sarkar, Daren L. Knoell, Estelle Cormet-Boyaka, Mark D. Wewers, Jonathan P. Butchar, Susheela Tridandapani

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Burkholderia cenocepacia, the causative agent of cepacia syndrome, primarily affects cystic fibrosis patients, often leading to death. In the lung, epithelial cells serve as the initial barrier to airway infections, yet their responses to B. cenocepacia have not been fully investigated. Here, we examined the molecular responses of human airway epithelial cells to B. cenocepacia infection. Infection led to early signaling events such as activation of Erk, Akt, and NF-κB. Further, TNFα, IL-6, IL-8, and IL-lβ were all significantly induced upon infection, but no IL-lβ was detected in the supernatants. Because caspase-1 is required for IL-lβ processing and release, we examined its expression in airway epithelial cells. Interestingly, little to no caspase-1 was detectable in airway epithelial cells. Transfection of caspase-1 into airway epithelial cells restored their ability to secrete IL-lβ following B. cenocepacia infection, suggesting that a deficiency in caspase-1 is responsible, at least in part, for the attenuated IL-lβ secretion.

Original languageEnglish (US)
Pages (from-to)3691-3695
Number of pages5
JournalJournal of Biological Chemistry
Volume288
Issue number6
DOIs
StatePublished - Feb 8 2013

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Gillette, D. D., Shah, P. A., Cremer, T., Gavrilin, M. A., Besecker, B. Y., Sarkar, A., Knoell, D. L., Cormet-Boyaka, E., Wewers, M. D., Butchar, J. P., & Tridandapani, S. (2013). Analysis of human bronchial epithelial cell proinflammatory response to Burkholderia cenocepacia infection: Inability to secrete IL-1 β. Journal of Biological Chemistry, 288(6), 3691-3695. https://doi.org/10.1074/jbc.C112.430298