The kallikrein-kininogen-kinin system in chronic inflammation

R. M. Burch, J. R. Connor, C. W. Tiffany

Research output: Contribution to journalArticle

Abstract

We examined bradykinin's effects on macrophages and fibroblasts, two cell types important in the pathogenesis of chronic inflammation. Bradykinin stimulated release of proteins of 18 kDa from macrophages. These proteins caused increased thymocyte proliferation (interleukin 1, IL-1) and completely inhibited lipoprotein lipase (tumor necrosis factor, TNF). When fibroblasts were incubated with bradykinin, PGE2 synthesis was stimulated. Pretreatment with IL-1 or TNF dramatically amplified bradykinin-stimulated PGE2 synthesis. Thus, bradykinin is involved in a positive feedback loop in which bradykinin activates macrophages to release potent inflammatory cytokines; these in turn amplify responsiveness of bradykinin target tissues.

Original languageEnglish (US)
Pages (from-to)258-260
Number of pages3
JournalAgents and Actions
Volume27
Issue number3-4
DOIs
StatePublished - Jun 1 1989

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology (medical)

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    Burch, R. M., Connor, J. R., & Tiffany, C. W. (1989). The kallikrein-kininogen-kinin system in chronic inflammation. Agents and Actions, 27(3-4), 258-260. https://doi.org/10.1007/BF01972790