C3A binds to the seven transmembrane anaphylatoxin receptor expressed by epithelial cells and triggers the production of IL-8

FEBS Lett. 2001 Jan 5;487(3):339-46. doi: 10.1016/s0014-5793(00)02320-6.

Abstract

The complement (C) plays an important role in many acute inflammatory processes. C3a is an inflammatory polypeptide named anaphylatoxin, generated during C activation and which acts through a specific receptor C3aR. In this study, we demonstrated that the epithelial cell line ECV 304 constitutively expressed C3aR (by flow cytometry and immunofluorescence) and that binding of purified C3a to epithelial cells resulted in a time- and dose-dependent upregulation of interleukin-8 (IL-8). Pre-treatment of ECV 304 with pertussis toxin inhibited IL-8 response induced by C3a, indicating that the action of C3a was mediated by a G protein coupled pathway.

MeSH terms

  • Anaphylatoxins / metabolism*
  • Anaphylatoxins / pharmacology
  • Base Sequence
  • Cell Line
  • Complement C3a / metabolism*
  • Complement C3a / pharmacology
  • DNA Primers / genetics
  • Epithelial Cells / drug effects
  • Epithelial Cells / immunology
  • Epithelial Cells / metabolism
  • GTP-Binding Proteins / metabolism
  • Gene Expression / drug effects
  • Humans
  • Interleukin-8 / biosynthesis*
  • Macrophage-1 Antigen / chemistry*
  • Macrophage-1 Antigen / genetics
  • Macrophage-1 Antigen / metabolism*
  • Pertussis Toxin
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Anaphylatoxins
  • DNA Primers
  • Interleukin-8
  • Macrophage-1 Antigen
  • RNA, Messenger
  • Virulence Factors, Bordetella
  • Complement C3a
  • Pertussis Toxin
  • GTP-Binding Proteins