Endogenous regulation of the acute inflammatory response
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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-кB 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-кB activation by interfering with breakdown of IKBa, while SLPI likewise suppresses NF-кB activation, but by interfering with breakdown of IKBß. Antibody induced blockade of IL-10, IL-13 or SLPI enhances NF-кB 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. (Mol Cell Biochem 234/235: 225–228, 2002)
KeywordsNF-KB inflammation lung injury neutrophils
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