• Mol. Cell. Biochem. · May 2002

    Review

    Endogenous regulation of the acute inflammatory response.

    • Peter A Ward and Alex B Lentsch.
    • Department of Pathology, University of Michigan, Ann Arbor 48109, USA. pward@umich.edu
    • Mol. Cell. Biochem. 2002 May 1;234-235(1-2):225-8.

    AbstractThe 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-kappaB 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-kappaB activation by interfering with breakdown of IkappaBalpha, while SLPI likewise suppresses NF-kappaB activation, but by interfering with breakdown of IkappaBbeta. Antibody induced blockade of IL-10, IL-13 or SLPI enhances NF-KB 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.

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