Evidence of IL-18 as a novel angiogenic mediator

J Immunol. 2001 Aug 1;167(3):1644-53. doi: 10.4049/jimmunol.167.3.1644.

Abstract

Angiogenesis, or new blood vessel growth, is a key process in the development of synovial inflammation in rheumatoid arthritis (RA). Integral to this pathologic proliferation are proinflammatory cytokines. We hypothesized a role for IL-18 as an angiogenic mediator in RA. We examined the effect of human IL-18 on human microvascular endothelial cell (HMVEC) migration. IL-18 induced HMVEC migration at 1 nM (p < 0.05). RA synovial fluids potently induced endothelial cell migration, but IL-18 immunodepletion resulted in a 68 +/- 5% decrease in HMVEC migration (p < 0.05). IL-18 appears to act on HMVECs via alpha(v)beta(3) integrin. To test whether IL-18 induced endothelial cell tube formation in vitro, we quantitated the degree of tube formation on Matrigel matrix. IL-18, 1 or 10 nM, resulted in a 77% or 87% increase in tube formation compared with control (p < 0.05). To determine whether IL-18 may be angiogenic in vivo, we implanted IL-18 in Matrigel plugs in mice, and IL-18 at 1 and 10 nM induced angiogenesis (p < 0.05). The angiogenesis observed appears to be independent of the contribution of local TNF-alpha, as evidenced by adding neutralizing anti-TNF-alpha Ab to the Matrigel plugs. In an alternative in vivo model, sponges embedded with IL-18 or control were implanted into mice. IL-18 (10 nM) induced a 4-fold increase in angiogenesis vs the control (p < 0.05). These findings support a novel function for IL-18 as an angiogenic factor in RA and may elucidate a potential therapeutic target for angiogenesis-directed diseases.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Angiogenesis Inducing Agents / antagonists & inhibitors
  • Angiogenesis Inducing Agents / immunology
  • Angiogenesis Inducing Agents / physiology*
  • Animals
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / pathology
  • Cell Division / immunology
  • Cell Line
  • Cell Migration Inhibition
  • Cell Movement / immunology
  • Chemokine CXCL5
  • Chemokines / physiology
  • Chemokines, CXC*
  • Chemotactic Factors / physiology
  • Collagen / administration & dosage
  • Drug Combinations
  • Drug Implants
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / growth & development
  • Endothelium, Vascular / immunology
  • Granuloma / physiopathology
  • Humans
  • Immune Sera / pharmacology
  • Interleukin-18 / administration & dosage
  • Interleukin-18 / antagonists & inhibitors
  • Interleukin-18 / immunology
  • Interleukin-18 / physiology*
  • Interleukin-8 / analogs & derivatives
  • Interleukin-8 / physiology
  • Laminin / administration & dosage
  • Mice
  • Mice, Inbred C57BL
  • Neovascularization, Physiologic / immunology
  • Porifera
  • Proteoglycans / administration & dosage
  • Receptors, Vitronectin / physiology
  • Recombinant Proteins / antagonists & inhibitors
  • Recombinant Proteins / immunology
  • Recombinant Proteins / pharmacology
  • Synovial Fluid / immunology
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Angiogenesis Inducing Agents
  • CXCL5 protein, human
  • Chemokine CXCL5
  • Chemokines
  • Chemokines, CXC
  • Chemotactic Factors
  • Drug Combinations
  • Drug Implants
  • Immune Sera
  • Interleukin-18
  • Interleukin-8
  • Laminin
  • Proteoglycans
  • Receptors, Vitronectin
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • matrigel
  • Collagen