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Mediators of Inflammation
Volume 13, Issue 3, Pages 205-207
http://dx.doi.org/10.1080/09511920410001713484

Involvement of fractalkine and macrophage inflammatory protein-1 alpha in moderate-severe depression

1Chair of Immunopathology, Department of Human Pathology, University of Messina, Italy
2Department of Pediatrics Science, University of Messina, Italy
3School and Division of Neurology, Department of Neurosciences, University of Messina, Italy
4Department of Neurosciences, Psychiatry and Anesthesiology, University of Messina, Italy
5SPDC, Azienda Ospedaliera Bianchi-Melacrino-Morelli, Reggio Calabria, Italy
6Bone Marrow Transplant Unit, Azienda Ospedaliera Bianchi-Melacrino-Morelli, Reggio Calabria, Italy
7School of Allergy and Clinical Immunology, Department of Human Pathology, University of Messina, Italy

Copyright © 2004 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.

Abstract

MODERATE-severe depression (MSD) is linked to overexpression of proinflammatory cytokines and chemokines. Fractalkine (FKN) and macrophage inflammatory protein-1 alpha (MIP-1α) are, respectively, members of CX3C and C-C chemokines, and both are involved in recruiting and activating mononuclear phagocytes in the central nervous system. We analysed the presence of FKN and MIP-1α in sera of untreated MSD patients and healthy donors. High FKN levels were observed in all MSD patients as compared with values only detectable in 26% of healthy donors. MIP-1α was measurable in 20% of patients, while no healthy donors showed detectable chemokine levels. In conclusion, we describe a previously unknown involvement of FKN in the pathogenesis of MSD, suggesting that FKN may represent a target for a specific immune therapy of this disease.