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Abstract Details

Correlation between Oxidatives Stress and Chemokines in the Cerebrospinal Fluid of Multiple Sclerosis Patients
MS and Related Diseases
P03 - (-)
232
BACKGROUND: Chemokines have been shown to modulate generation of reactive oxygen species (ROS) at the site of inflammation. This association between ROS and inflammation, was viewed as a one-way process, i.e. immune cells activated by chemokines produced ROS. However, excessive ROS production disturbs redox status, damages macromolecules, and can modulate the expression of a variety of immune and inflammatory molecules, exacerbating inflammation and affecting tissue damage. The aim of the current study is to establish a relationship between oxidative stress and chemokines with disease activity in MS.
DESIGN/METHODS: Spinal fluid was obtained from 25 patients with clinically definite MS and 10 control pateints with other neurological disease with consent under an IRB-approved protocol. CSF was examined to ensure absence of red blood cell contamination and stored at -80 degree until use. Chemokines profiles in CSF were evaluated using the Multi-Analyte ELISArray kit from Qiagen. Oxidative stress was measured using biomarkers for lipid peroxidation - isoprostanes (IsoPs) and malondialdehyde (MDA). Oxidized glutathione (GSSG) as well as the total anti-oxidant status (TAS) in CSF was also determined.
RESULTS: We found significantly increased levels of the chemokines - IL-8/CXCL8, MCP-1/CCL2 and IP-10/CXCL10 in the MS CSF samples with increased oxidative stress (p <0.02). These chemokines were not increased in the CSF of the control samples with no measurable oxidative stress. Furthermore, our results show depleted TAS levels in the MS samples with increased chemokines and oxidative stress. The correlation between chemokines and the oxidative stress markers was found to be highest in the secondary progressive MS patient group.
CONCLUSIONS: These findings indicate a positive interaction between chemokines and oxidative stress in MS. Further investigation may better our understanding of pathology and lead to improvement in therapy.
Authors/Disclosures

PRESENTER
No disclosure on file
Donald Lee No disclosure on file
No disclosure on file
Saud Sadiq, BS, FAAN (Tisch Multiple Sclerosis Research Center of New York) Ms. Brewi has nothing to disclose.
Janet Benesh, BSMT (Abbott Laboratories) No disclosure on file