Search

Obesity is a possible risk factor of multiple sclerosis (MS), but the association between obesity and MS disease activity has not been explored. In a cohort of 86 MS patients, 80% of overweight or obese patients (BMI ≥ 25 kg/m 2 ) had MRI activity compared to 48% of the normal-weight patients (BMI < 25 kg/m 2 ) (p = 0.001) during interferon-beta treatment. NEDA-status (no evidence of disease activity) was defined as a composite that consisted of absence of any relapses, sustained disability-progression and MRI-activity. Among normal-weight patients 26% obtained NEDA-status compared to only 13% of patients with BMI > 25 (p = 0.05). This may indicate that BMI affects interferon-beta treatment response. [ABSTRACT FROM AUTHOR]

Abstract: The purpose of the current study is to examine the surface expression of chemokine receptors and the chemotaxis toward the respective chemokines of glatiramer acetate (GA)–specific CD4+ T cells isolated from the blood and the cerebrospinal fluid (CSF) of a multiple sclerosis (MS) patient. Four clones were selected, two isolated from the peripheral blood and two from the CSF. CCR4 and CXCR3 were expressed on all four clones. Both blood-derived clones also expressed CCR5 and, to a lesser extent, CCR6. Similarly, one CSF clone expressed CCR5 and CCR6. In contrast, CCR1, CCR2, CCR3, CCR7, CCR9, CCR10, CXCR1, CXCR4, CXCR5, CXCR6, and CCR6 were either expressed on few cells or were not expressed at all on all four clones examined. The expression of chemokine receptors was corroborated with the ability of the cells to respond chemotactically to the corresponding chemokines, CCL5/RANTES, CCL20/MIP-3α, CCL22/MDC and CXCL10/IP-10. Both the receptor expression and chemotaxis were reduced upon activation with PMA and ionomycin. The shared expression of chemokine receptors and the migration patterns suggest that GA-reactive cells have migrated from the blood into the CSF, and that local reactivation within the inflamed CSF may downregulate the expression of chemokine receptors and hence impede their migration intrathecally. The results may also explain the beneficial synergistic effects of combining immunosuppressive drugs with GA in MS patients. [ABSTRACT FROM AUTHOR]

Abstract: To explore the relationships between vitamin A, D and E and inflammation in relapsing remitting multiple sclerosis, we assessed their associations with 11 inflammation markers in 9 serial serum samples from 85 patients, before and during interferon-β1a treatment. A negative association was found between vitamin A and pentraxin 3 independent of interferon-β1a use, whereas positive associations between vitamin D and interleukin-1 receptor antagonist and secreted frizzled-related protein 3 were seen before, and between vitamin E and chemokine (C-X-C motif) ligand 16 during interferon-β1a treatment. These findings suggest associations with diverse inflammatory pathways, which may be differentially influenced by interferon-β1a treatment. [Copyright &y& Elsevier]

Abstract: Calprotectin is produced by activated monocytes and microglia, and cerebrospinal fluid (CSF) levels could be a marker of neuroinflammation. Calprotectin was detectable in CSF from 13.8% of normal controls, compared to 90.5% of patients with neurological infections (p <0.001). In CSF from patients with multiple sclerosis (MS) and clinically isolated demyelinating syndrome, calprotectin was detected in 64.7% within 2weeks after symptom debut compared to 30.8% between 2 and 4weeks and 17.0% thereafter (p <0.001). We conclude that CSF calprotectin reflects the disease activity in MS but does not discriminate between MS and other inflammatory or infectious conditions. [Copyright &y& Elsevier]