Effect of annexin-1 on experimental autoimmune encephalomyelitis (EAE) in the rat.

Authors: Huitinga, I  Bauer, J  Strijbos, PJ  Rothwell, NJ  Dijkstra, CD  Tilders, FJ 
Citation: Huitinga I, etal., Clin Exp Immunol. 1998 Jan;111(1):198-204.
Pubmed: (View Article at PubMed) PMID:9472682

Annexin-1, a calcium-dependent phospholipid binding protein, has been shown to act as an endogenous central neuroprotectant, notably against cerebral ischaemic damage. In the present study we extend these findings to an animal model of multiple sclerosis, EAE, and report that endogenous annexin-1 is expressed in ED1+ macrophages and resident astrocytes localized within the lesions in the central nervous system (CNS). Intracerebroventricular (i.c.v.) administration of an NH2-terminal fragment spanning amino acids 1-188 of annexin-1 after the onset of the clinical symptoms significantly reduced both the neurological severity as well as weight loss of mild EAE. Immunoneutralization of endogenous brain annexin-1 failed to exacerbate the clinical features of EAE. Thus, although the role of endogenous annexin-1 in the pathogenesis of EAE remains to be determined, our findings suggest that annexin-1 may be of therapeutic benefit to the treatment of multiple sclerosis.

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CRRD ID: 2306942
Created: 2009-05-12
Species: All species
Last Modified: 2009-05-12
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.