mob-1 Expression in IL-2-induced ARDS: Regulation by TNF-α

L. F. Neville*, F. Abdullah, P. M. McDonnell, P. R. Young, G. Z. Feuerstein, R. Rabinovici

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

We have recently established an animal model of adult respiratory distress syndrome (ARDS)-like microvascular lung injury elicited by infusion of human interleukin-2 (IL-2). Based on the pronounced, transcriptional upregulation of multiple pro-inflammatory mediators in IL-2-induced ARDS, differential display was applied to search for potentially novel genes in this paradigm of lung injury. Differential display on total lung RNA derived from IL-2- challenged rats presented a highly reproducible 3'-UTR fragment profile in which a band (≃250 bp), termed B1, was strongly induced. B1 cDNA sequence exhibited 99.14% homology to the 3'-UTR of mob-1, a recently cloned gene belonging to the C-X-C chemokine superfamily. Furthermore, Northern blot analysis showed that IL-2-induced pulmonary mob-1 mRNA was expressed at time points before the onset of lung injury and suppressed after TNF-α inhibition. These data imply that lung mob-1 is a novel, highly inducible gene in a clinically relevant model of ARDS and, based on its identification as a chemokine, could participate in the development of lung injury.

Original languageEnglish (US)
Pages (from-to)L884-L890
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume269
Issue number6 13-6
DOIs
StatePublished - 1995

Keywords

  • adult respiratory distress syndrome
  • chemokine
  • differential display
  • interleukin-2
  • lung injury
  • tumor necrosis factor- α

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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