Regulatory effects of interleukin-11 during acute lung inflammatory injury

Alex B. Lentsch, Larry D. Crouch, Jacqueline A. Jordan, Boris J. Czermak, Edward C. Yun, Guo Renfeng, Vidya Sarma, Kathleen M. Diehl, Peter A. Ward

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


The role of interleukin-11 (IL-11) was evaluated in the IgG immune complex model of acute lung injury in rats. IL-11 mRNA and protein were both up-regulated during the course of this inflammatory response. Exogenously administered IL-11 substantially reduced, in a dose-dependent manner, the intrapulmonary accumulation of neutrophils and the lung vascular leak of albumin. These in vivo anti-inflammatory effects of IL-11 were associated with reduced NF-κB activation in lung, reduced levels of tumor necrosis factor α (TNF-α) in bronchoalveolar lavage (BAL) fluids, and diminished up- regulation of lung vascular ICAM-1. It is interesting that IL-11 did not affect BAL fluid content of the CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-inducible neutrophil chemoattractant (CINC); the presence of IL-11 did not affect these chemokines. However, BAL content of C5a was reduced by IL-11. These data indicate that IL-11 is a regulatory cytokine in the lung and that, like other members of this family, its anti- inflammatory properties appear to be linked to its suppression of NF-κB activation, diminished production of TNF-α, and reduced up-regulation of lung vascular ICAM-1.

Original languageEnglish (US)
Pages (from-to)151-157
Number of pages7
JournalJournal of Leukocyte Biology
Issue number1
StatePublished - 1999


  • C5α
  • Chemokines
  • ICAM-1
  • NF-κB
  • Neutrophils
  • Tumor necrosis factor α

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology


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