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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Interleukin-13 Modulates Collagen Homeostasis in Human Skin and Keloid Fibroblasts

Alfonso Oriente, Neal S. Fedarko, Sarah E. Pacocha, Shau-Ku Huang, Lawrence M. Lichtenstein and David M. Essayan
Journal of Pharmacology and Experimental Therapeutics March 2000, 292 (3) 988-994;
Alfonso Oriente
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Neal S. Fedarko
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Sarah E. Pacocha
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Shau-Ku Huang
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Lawrence M. Lichtenstein
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David M. Essayan
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Abstract

Interleukin (IL)-13 has been implicated in the pathogenesis of various diseases characterized by fibrosis. We describe the effects of IL-13 on collagen homeostasis from normal (NF) and keloid (KF) fibroblasts and compare these effects with those of IL-4 and transforming growth factor (TGF)-β1. Total collagen generation was up-regulated in NF after 48 h of stimulation by IL-13; in KF, IL-13 stimulated a more rapid collagen response. The kinetics and magnitude of collagen generation induced by IL-13 were equivalent to those induced by similar concentrations of IL-4 and TGF-β1. Collagen type I production paralleled total collagen generation from both NF and KF; however, IL-4-induced collagen type I and total collagen production from KF was more transient than that induced by either IL-13 or TGF-β1. Procollagen 1α1 gene expression was induced in KF by stimulation with IL-13 for 24 h. Moreover, IL-13 was unique among these three cytokines in its ability to induce gene expression for procollagen 3α1. Finally, IL-13 inhibited IL-1β-induced matrix metalloproteinase (MMP)-1 and MMP-3 production and enhanced tissue inhibitor of metalloproteinase (TIMP)-1 generation from NF; although similar effects were observed with IL-4, TGF-β1transiently enhanced MMP-1 and MMP-3 generation without effecting TIMP-1. In KF, IL-13 and IL-4 inhibited MMP-3, whereas TGF-β1 enhanced MMP-3; TIMP-1 was unaffected by any of the three cytokines. These data demonstrate both the profibrotic effects of IL-13 on collagen homeostasis and the potential differential regulation of collagen homeostasis in fibroblast subtypes by IL-13.

Footnotes

  • Send reprint requests to: David M. Essayan, M.D., The Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Room 1A12, Baltimore, MD 21224. E-mail:dessayan{at}jhmi.edu

  • 1 This work was supported by grants AI34002 and AI07290 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health.

  • Abbreviations:
    ECM
    extracellular matrix
    KF
    keloid fibroblast
    MMP
    matrix metalloproteinase
    NF
    normal fibroblast
    Col1α
    procollagen 1α1
    Col3α
    procollagen 3α1
    OH-Pro
    hydroxyproline
    IL
    interleukin
    TGF
    transforming growth factor
    PCR
    polymerase chain reaction
    RT
    reverse transcription
    TIMP
    tissue inhibitor of metalloproteinase
    • Received July 16, 1999.
    • Accepted November 8, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 292 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 292, Issue 3
1 Mar 2000
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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Interleukin-13 Modulates Collagen Homeostasis in Human Skin and Keloid Fibroblasts

Alfonso Oriente, Neal S. Fedarko, Sarah E. Pacocha, Shau-Ku Huang, Lawrence M. Lichtenstein and David M. Essayan
Journal of Pharmacology and Experimental Therapeutics March 1, 2000, 292 (3) 988-994;

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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Interleukin-13 Modulates Collagen Homeostasis in Human Skin and Keloid Fibroblasts

Alfonso Oriente, Neal S. Fedarko, Sarah E. Pacocha, Shau-Ku Huang, Lawrence M. Lichtenstein and David M. Essayan
Journal of Pharmacology and Experimental Therapeutics March 1, 2000, 292 (3) 988-994;
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