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Autocrine action of IL-10 suppresses proinflammatory mediators and inflammation in the HSV-1-infected cornea.

Abstract
We investigated whether IL-10 produced endogenously would influence the development of HSV-1-induced acute corneal disease. Murine corneal epithelial cells and fibroblasts cultured in vitro expressed IL-10 mRNA and protein constitutively and also IL-10 receptors. Inclusion of IL-10 neutralizing antibody in the culture medium significantly (p<0.05) enhanced TNF-alpha-induced IL-6 and MIP-2 production by both corneal cell types. Endogenous IL-10 synthesis, which also occurred in vivo, was not modulated by Herpes virus infection or by depletion of neutrophils or natural killer cells. Antibody to IL-10 given locally at the time of HSV-1 intracorneal infection was associated with significantly (p<0.05) enhanced production of IL-6, MIP-2, and MIP-1alpha, increased neutrophil infiltration, and more extensive corneal disease. Similarly, mice with a disrupted IL-10 gene developed more severe corneal disease than wild-type controls. Collectively, these observations suggest that locally produced IL-10 can act in an autocrine/paracrine fashion to down-regulate the production of proinflammatory mediators and thus limit corneal inflammation.
AuthorsX T Yan, M Zhuang, J E Oakes, R N Lausch
JournalJournal of leukocyte biology (J Leukoc Biol) Vol. 69 Issue 1 Pg. 149-57 (Jan 2001) ISSN: 0741-5400 [Print] United States
PMID11200059 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Interleukin-10
Topics
  • Animals
  • Autocrine Communication (immunology)
  • Cornea (immunology, virology)
  • Corneal Diseases (immunology, virology)
  • Female
  • Herpes Simplex (immunology)
  • Herpesvirus 1, Human (immunology)
  • Inflammation (immunology)
  • Interleukin-10 (immunology)
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout

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