Multiple Sclerosis Inflammation May Play a Role in Healthy Individuals
Better understanding the relationship between inflammation and biomarkers could help improve treatments for those with multiple sclerosis.
Better understanding the relationship between inflammation and biomarkers could help improve treatments for those with multiple sclerosis.
Previous research has found evidence determining that central nervous system (CNS) degeneration depends on inflammation in patients with relapsing-remitting multiple sclerosis (RRMS). Cerebrospinal fluid (CSF) biomarkers appear to reveal if disease modifying therapies (DMT) are reducing disease activity. Lenka Nováková, of the Sahlgrenska University Hospital in Sweden, and colleagues explored the connection further and will explain the findings in a poster session at the 31st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS 2015) in Barcelona, Spain.
The researchers examined 72 patients with RRMS and 39 healthy controls. For the patients with RRMS, 68 were on DMT (36 interferon beta, 19 natalizumab, nine glatiramer acetate (GA), two teriflunomide, two intravenous immunoglobulin) and four were treatment-native. The data focused on:
- B-cell activity (CXCL13)
- Monocyte/memory T-cell/dendritic cell recruitment (monocyte chemotactic protein 1, MCP1)
- Glial activation (chitinase 3-like 1 or YKL-40)
- Astrogliosis (glial fibrillary acidic protein, GFAP)
- Axonal damage (neurofilament light protein, NFL) in CSF by ELISA
The results showed that compared to the healthy controls, those with RRMS had higher levels of CXCL13, YKL-40, and NFL. In addition, the 47 patients with RRMS who were treated with first line therapies, such as interferon beta, GA, and teriflunomide, had higher levels of CXCL13 and NFL than the 19 patients treated with natalizumab.
“With few exceptions, the interrelation analysis of the biomarkers in RRMS showed significant correlations between inflammatory and degenerative biomarkers. The strongest relationships were found between YKL-40 and GFAP and NFL (r=0.426, p<0.001 and r=0.689, p<0.001, respectively),” the authors confirmed.
They continued to explain that, “Interestingly, similar and even stronger correlations were found for these biomarkers in [healthy controls].” This suggests that although research continues to support that patients with RRMS have increased YKL-40, which is linked to MS inflammation, it seems that it may also have other roles in healthy individuals.
