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

FEBS Letters

Fontaine, Marc²  Ischenko, Alexander¹  Monsinjon, Tiphaine²  Gasque, Philippe³ 

[1] RIHPB (Research Institute of Highly Pure Biopreparations), Saint Petersburg, Russia;Faculté Mixte de Médecine/Pharmacie, INSERM U519, 22 Boulevard Gambetta, 76183 Rouen Cedex, France;Brain Inflammation and Immunity Group, Department of Medical Biochemistry and Pathology, University of Wales, Cardiff, UK

关键词: Complement;    C3a receptor;    Anaphylatoxin;    Epithelial cell;    Interleukin-8;    Ab;    antibody;    BSA;    bovine serum albumin;    C;    complement;    C3aR;    C3a receptor;    C5aR;    C5a receptor;    FACS;    fluorescence analysis cell sorter;    GAPDH;    glyceraldehyde 3-phosphate dehydrogenase;    IF;    immunofluorescence;    IL;    interleukin;    MMLV;    Moloney murine leukaemia virus;    PBS;    phosphate-buffered saline;    PE;    phycoerythrine;    PMA;    phorbol myristate acetate;    PTX;    pertussis toxin;    RT-PCR;    reverse transcription-polymerase chain reaction;   

DOI  :  10.1016/S0014-5793(00)02320-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown