Expression and contribution of endogenous IL-13 in an experimental model of sepsis

Akihiro Matsukawa, Cory M. Hogaboam, Nickolas W. Lukacs, Pamela M. Lincoln, Holly L. Evanoff, Robert M. Strieter, Steven L. Kunkel

Research output: Contribution to journalArticle

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Abstract

IL-13 has been shown to exert potent anti-inflammatory properties. In this study, we elucidated the functional role of endogenous IL-13 in a murine model of septic peritonitis induced by cecal ligation and puncture (CLP). Initial studies demonstrated that the level of IL-13 increased in tissues including liver, lung, and kidney, whereas no considerable increase was found in either peritoneal fluid or serum after CLP. Immunohistochemically, IL-13- positive cells were Kupffer cells in liver, alveolar macrophages in lung, and epithelial cells of urinary tubules in kidney. IL-13 blockade with anti-IL-13 Abs significantly decreased the survival rate of mice after CLP from 53% to 14% on day 7 compared with control. To determine the potential mechanisms whereby IL-13 exerted a protective role in this model, the effects of anti- IL-13 Abs on both local and systemic inflammation were investigated. Administration of anti-IL-13 Abs did not alter the leukocyte infiltration and bacterial load in the peritoneum after CLP but dramatically increased the neutrophil influx in tissues after CLP, an effect that was accompanied by significant increases in the serum levels of aspartate transaminase, alanine transaminase, blood urea nitrogen, and creatinine. Tissue injury caused by IL-13 blockade was associated with increases in mRNA and the protein levels of CXC chemokines macrophage inflammatory protein-2 and KC as well as the CC chemokine macrophage inflammatory protein-1α and the proinflammatory cytokine TNF-α. Collectively, these results suggest that endogenous IL-13 protected mice front CLP-induced lethality by modulating inflammatory responses via suppression of overzealous production of inflammatory cytokines/chemokines in tissues.

Original languageEnglish
Pages (from-to)2738-2744
Number of pages7
JournalJournal of Immunology
Volume164
Issue number5
Publication statusPublished - Mar 1 2000
Externally publishedYes

Fingerprint

Interleukin-13
Sepsis
Theoretical Models
Punctures
Ligation
Chemokine CXCL2
Kidney Tubules
Cytokines
Macrophage Inflammatory Proteins
CXC Chemokines
CC Chemokines
Lung
Kupffer Cells
Bacterial Load
Ascitic Fluid
Liver
Peritoneum
Blood Urea Nitrogen
Alveolar Macrophages
Aspartate Aminotransferases

ASJC Scopus subject areas

  • Immunology

Cite this

Matsukawa, A., Hogaboam, C. M., Lukacs, N. W., Lincoln, P. M., Evanoff, H. L., Strieter, R. M., & Kunkel, S. L. (2000). Expression and contribution of endogenous IL-13 in an experimental model of sepsis. Journal of Immunology, 164(5), 2738-2744.

Expression and contribution of endogenous IL-13 in an experimental model of sepsis. / Matsukawa, Akihiro; Hogaboam, Cory M.; Lukacs, Nickolas W.; Lincoln, Pamela M.; Evanoff, Holly L.; Strieter, Robert M.; Kunkel, Steven L.

In: Journal of Immunology, Vol. 164, No. 5, 01.03.2000, p. 2738-2744.

Research output: Contribution to journalArticle

Matsukawa, A, Hogaboam, CM, Lukacs, NW, Lincoln, PM, Evanoff, HL, Strieter, RM & Kunkel, SL 2000, 'Expression and contribution of endogenous IL-13 in an experimental model of sepsis', Journal of Immunology, vol. 164, no. 5, pp. 2738-2744.
Matsukawa A, Hogaboam CM, Lukacs NW, Lincoln PM, Evanoff HL, Strieter RM et al. Expression and contribution of endogenous IL-13 in an experimental model of sepsis. Journal of Immunology. 2000 Mar 1;164(5):2738-2744.
Matsukawa, Akihiro ; Hogaboam, Cory M. ; Lukacs, Nickolas W. ; Lincoln, Pamela M. ; Evanoff, Holly L. ; Strieter, Robert M. ; Kunkel, Steven L. / Expression and contribution of endogenous IL-13 in an experimental model of sepsis. In: Journal of Immunology. 2000 ; Vol. 164, No. 5. pp. 2738-2744.
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