Endogenous regulation of the acute inflammatory response
- 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.