Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 221, Issue 1-2, Pages 46-52Publisher
ELSEVIER
DOI: 10.1016/j.jneuroim.2010.02.011
Keywords
Inflammation; Complement system; Anaphylatoxins; Brain; Systemic lupus erythematosus
Categories
Funding
- National Institutes of Health [R01DK055357]
- American Heart Association [0855717G]
Ask authors/readers for more resources
To investigate the role of C5a generated on complement activation in brain, the lupus model, MRL/lpr mice were treated with C5a receptor(R) antagonist (ant). Neutrophil infiltration, ICAM, TNF-alpha and iNOS mRNA expression, neuronal apoptosis and the expression of p-JNK, pSTAT1 and p-Erk were reduced and p-Akt increased on C5aR inhibition in MRL/lpr brains. MRL/lpr serum caused increased apoptosis in neurons showing that lupus had a direct effect on these cells. C5aRant pretreatment prevented the lupus serum induced loss of neuronal cells. Our findings demonstrate for the first time that C5a/C5aR signaling plays an important role in the pathogenesis of CNS lupus. (C) 2010 Published by Elsevier B.V.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available