Molecular and Cellular Biochemistry

, Volume 234, Issue 1, pp 225–228

Endogenous regulation of the acute inflammatory response

  • Peter A. Ward
  • Alex B. Lentsch

DOI: 10.1023/A:1015944709177

Cite this article as:
Ward, P.A. & Lentsch, A.B. Mol Cell Biochem (2002) 234: 225. doi:10.1023/A:1015944709177


The acute inflammatory response has been triggered in rat lungs by deposition of IgG immune complexes. The inflammatory reaction triggered is highly tissue damaging and requires activation of NF-κB with ensuing generation of chemokines and cytokines. Endogenous generation of IL-10 and IL-13 as well as secretory leukocyte protease inhibitor (SLPI), significantly regulates this inflammatory response. IL-10 and IL-13 attenuate NF-κB activation by interfering with breakdown of IκBα, while SLPI likewise suppresses NF-κB activation, but by interfering with breakdown of IκBβ. Antibody induced blockade of IL-10, IL-13 or SLPI enhances NF-κB activation in lung and exacerbates the lung inflammatory response and injury. These data indicate that endogenous IL-10, IL-13 and SLPI are important regulators of the inflammatory response by reducing gene activation with resultant generation of peptide mediators/cytokines and chemokines.

NF-κB inflammation lung injury neutrophils 

Copyright information

© Kluwer Academic Publishers 2002

Authors and Affiliations

  • Peter A. Ward
    • 1
  • Alex B. Lentsch
    • 1
  1. 1.Department of PathologyUniversity of MichiganAnn ArborUSA

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