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Oxygen/Nitrogen Radicals: Cell Injury and Disease pp 225–228Cite as

Endogenous regulation of the acute inflammatory response

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Part of the book series: Developments in Molecular and Cellular Biochemistry ((DMCB,volume 37))

Abstract

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)

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Authors and Affiliations

  1. Department of Pathology, University of Michigan, Ann Arbor, USA

    Peter A. Ward & Alex B. Lentsch

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  1. Peter A. Ward
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  2. Alex B. Lentsch
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Editors and Affiliations

  1. Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, 1095 Willowdale Road Mall Stop B167, Morgantown, WV, 26505, USA

    Val Vallyathan , Xianglin Shi Ph.D.  & Vince Castranova ,  & 

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© 2002 Springer Science+Business Media New York

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Ward, P.A., Lentsch, A.B. (2002). Endogenous regulation of the acute inflammatory response. In: Vallyathan, V., Shi, X., Castranova, V. (eds) Oxygen/Nitrogen Radicals: Cell Injury and Disease. Developments in Molecular and Cellular Biochemistry, vol 37. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1087-1_26

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  • DOI: https://doi.org/10.1007/978-1-4615-1087-1_26

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5388-1

  • Online ISBN: 978-1-4615-1087-1

  • eBook Packages: Springer Book Archive

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