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Mediators of Inflammation
Volume 2 (1993), Issue 2, Pages 109-113

Conceivable difference in the anti-inflammatory mechanisms of lipocortins 1 and 5

1Department of Molecular Biology, Immunobiological Research Institute Siena, Siena 53100, Italy
2Department of Pharmacology, Immunobiological Research Institute Siena, Siena 53100, Italy
3Department of Biochemical Pharmacology, The William Harvey Research Institute, St. Bartholomew's Hospital Medical School, Charterhouse Square, London EC1M 6BQ, UK

Received 6 January 1993; Accepted 21 January 1993

Copyright © 1993 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Human recombinant lipocortins (LCT) 1 and 5 have been expressed in a yeast secretion vector and purified by ion exchange chromatography. The action of the proteins has been investigated in two models of experimental acute inflammation in the rat: carrageenin induced paw oedema and zymosan induced pleurisy. The effects of the proteins on PGE2 release in vitro by rat macrophages stimulated with zymosan and on rat neutrophil chemotaxis induced by FMLP have also been assessed. LCT-1 significantly inhibited both paw swelling in carrageenin oedema and leukocyte migration in zymosan pleurisy. Moreover it showed a dose dependent, inhibitory effect on PGE2 release. Neutrophil chemotaxis was only weakly affected by LCT-1. Conversely LCT-5 did not reduce carrageenin oedema and slightly inhibited PGE2 release, but showed profound, dose dependent inhibitory activity on leukocyte migration in zymosan pleurisy and on neutrophil chemotaxis. These data suggest that LCT-1 acts mainly by interfering with arachidonic acid metabolism via the inhibition of phospholipase A2. The anti-inflammatory activity of LCT-5, at variance with LCT-1, may be due to a direct effect on cell motility in addition to the interference with arachidonic acid metabolism.