Regulation of chemokine expression by IL-10 in lung inflammation

Thomas P. Shanley*, Niti Vasi, Alvin Denenberg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

70 Scopus citations


We have been interested in understanding the mechanisms regulating the inflammatory process underlying acute lung injury. The current studies have employed a model of acute lung inflammation in mice triggered by bacterial lipopolysaccharide. The development of this injury was associated with increased expression of the chemokines, MIP-1α and MIP-2, that coordinate recruitment of neutrophils to the lung. IL-10 is a potent, endogenous anti-inflammatory molecule that has been shown to decrease lung inflammation partly on the basis of TNF-α and IL-1β inhibition. In these studies we tested the hypothesis that endogenous IL-10 modulates chemokine expression using the IL-10 knock-out mouse, and then explored the molecular mechanisms by which IL-10 might do so. The results demonstrate that significant elevations in both chemokines were observed in the absence of IL-10 and that these findings were associated with significant increases in lung neutrophil accumulation. In vitro studies defined two, gene-specific, mechanisms by which IL-10 regulated chemokine expression: mRNA destabilization and NF-κB inhibition. These results suggested that IL-10 is an important, endogenous regulator of chemokine expression in acute lung inflammation. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)1054-1064
Number of pages11
Issue number7
StatePublished - Jul 2000


  • Interleukin 10
  • Lung inflammation
  • MIP-1α
  • MIP-2
  • NF-κB
  • Neutrophils

ASJC Scopus subject areas

  • Molecular Biology
  • Hematology
  • Biochemistry
  • Immunology and Allergy
  • Immunology


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