C5a causes limited, polymorphonuclear cell-independent, mesenteric ischemia/reperfusion-induced injury
C5 is critical in the development of local mucosal damage and inflammation as well as in the development of remote organ injury after mesenteric ischemia/reperfusion (IR). To define the role of C5a in tissue injury, we treated wild-type mice with a cyclic hexapeptide C5a receptor antagonist (C5aRa)...
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 108(2003), 3 vom: 19. Sept., Seite 263-73 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , |
| Format: | Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2003
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Comparative Study Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Antigens, CD Complement C5 Complement Membrane Attack Complex Eicosanoids Receptor, Anaphylatoxin C5a Receptors, Complement mehr... |
| Zusammenfassung: | C5 is critical in the development of local mucosal damage and inflammation as well as in the development of remote organ injury after mesenteric ischemia/reperfusion (IR). To define the role of C5a in tissue injury, we treated wild-type mice with a cyclic hexapeptide C5a receptor antagonist (C5aRa) and administered recombinant C5a to C5 deficient (C5(-/-)) mice subjected to mesenteric IR. We demonstrate that at 2-h postreperfusion, C5a administered to C5-/- mice during IR induces limited intestinal mucosal injury but failed to cause remote lung injury despite the fact that it upregulated adhesion molecule expression. C5aRa treatment of C5+/+ mice undergoing IR limited local injury and prevented distant organ injury. We conclude that although C5a can trigger certain components of the IR induced injury, other mediators such as C5b-9 and local factors are needed for the complete expression of IR tissue damage |
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| Beschreibung: | Date Completed 30.10.2003 Date Revised 08.11.2019 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |