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Biomarkers and microRNA


Biomarker identified to measure MS severity(19/06/15)

In a study published in the journal Nature Communications, researchers have clarified the lifespan of antibody-producing cells and have also identified a novel biomarker that could be used to monitor autoimmune conditions such as multiple sclerosis and lupus erythematous.

The humoral immune response is mediated by cells in plasma and is responsible for fighting infections. Plasma cells secrete antibodies, proteins that are able to identify pathogens and destroy them. However, antibodies with specific characteristics sometimes attack their host tissues causing autoimmune conditions like multiple sclerosis (MS) or lupus erythematosus(SLE).

“Balanced regulation of the production and activity of plasma cells is therefore vital,” Professor Edgar Meinl of the LMU Medical Centre said.

The researchers were able to identify a mechanism of action involved in the regulation of these antibody producing cells’ lifespan. Specifically, the researchers found a cell-surface receptor, called BCMA, can be a useful biomarker for monitoring the severity of autoimmune diseases.

The cells in the plasma are produced by B-cells, which carry certain membrane-bound receptors that are able to identify antigens. When B-cells recognize an antigen, they are able to differentiate it into a clone of plasma cells that secrete the antigen-binding protein in soluble form as antibody. But the life-span of these antibodies is dependent on the BCMA receptor survival.

The extension of the lifespan of the plasma cells is activated by the BAFF and APRIL survival factors, BCMA ligands.. “However, the lifetime of plasma cells cannot be prolonged indefinitely. Otherwise the organism would become swamped with antibodies, increasing the risk of an autoimmune reaction,” Meinl explained.

“We have now shown, in cooperation with colleagues in Munich, Berlin and Stockholm, that the membrane-bound enzyme gamma-secretase acts as a brake on immune reactions by fragmenting BCMA.”

BCMA extended the cell’s membrane and is projected in the extracellular medium. Gamma-secretase removes the exposed portion by cutting the protein inside of the plasma membrane. That this enzyme cleaves the receptor directly was a surprise: “Up to now, it was only known to be involved in the degradation of membrane proteins that had already been cleaved by other enzymes.

“BCMA is the first natural substrate of gamma-secretase to be identified that is directly cleaved by the enzyme,” said Meinl, “and probably reflects the fact that the extracellular segment of the receptor is unusually short.”

The cleaved fragment is constant, and can be detected in fluid of the body as soluble BCMA (sBCMA). The evidence from this new study showed that in patients with Lupus, the sBCMA levels in the blood are high and associated correlated with the disease severity.

“In MS patients sBCMA levels were increased specifically in the cerebrospinal fluid, which bathes the brain and the spinal cord,” said Meinl. “So, sBCMA is an indicator of the intensity of ongoing immune reactions. sBCMA is therefore well suited to serve as an informative clinical parameter for the assessment of the therapeutic effects of different treatment regimes on plasma cells.”

Results from this study could trigger the development of treatments, with both B cells and the BCMA/BAFF/APRIL mechanism being targets for lupus and multiple sclerosis, treatment.

Soure: Multiple Sclerosis News Today © BioNews Services 2015 (19/06/15)

Uric acid correlated with multiple sclerosis disease activity(18/02/15)

In a study published in the journal Clinical Chemistry and Laboratory Medicine, investigators Moccia et al identified uric acid as a potential biomarker in the progression of multiple sclerosis-related disability.

Uric acid, which has activity as a natural scavenger of oxygen radicals, is present in the bloodstream as a breakdown product of purines (adenine and guanine). In animal studies, uric acid has been shown to have some potential as a treatment for MS. Results of these studies led investigators in the CCLM study to search for a relationship between MS severity and levels of uric acid. In the case-control study, using propensity score matching, investigators paired 362 patients with MS and 181 control individuals without MS.

To reduce variation between populations, investigators corrected data for patient age, gender, and kidney function. Upon regression analysis, investigators identified a significant association between low levels of serum uric acid among patients with MS compared with controls, with an R-squared value of 30.4 per cent and significance determined at a P value level of 1.4 per cent.

Longer disease duration was associated with a longer time from diagnosis and a higher Expanded Disability Status Scale (EDSS) score (P < .001, all comparisons). These findings suggest that uric acid levels may be a biomarker of MS disability and progression, even though previous studies suggest that uric acid may have a limited role as a disease marker and as a therapeutic target in MS.

For example, a 2006 analysis, published in the journal Clinical Neurology and Neurosurgery, found that uric acid levels did not change as a result of immunomodulatory or immunosuppressive drug treatment in patients with MS.

In addition, in the Association of Inosine and Interferon beta in relapsing- remitting Multiple Sclerosis (ASIIMS) trial, investigators administered a precursor of uric acid — inosine — to patients with MS in conjunction with interferon-beta over the course of two years. The results of this trial were negative, and uric acid did not have any additional benefit on disability outcomes versus interferon-beta alone.

Despite the negative result of the ASIIMS trial, antioxidative drugs may have a future in treatment of MS. However, uric acid may be a biomarker — not a treatment modality. Studying uric acid may help physicians predict the progression of MS in patients, although previous research indicates that uric acid levels do not predict response to treatment, and supplementation with uric acid does not alter the progression of disability in MS. Further study will be necessary to determine whether or not drugs that mimic the effects of uric acid are of any value.

Source: HCPLive Copyright HCPLive 2006-2013 Intellisphere, LLC (18/02/15)

The effects of microparticles on endothelial barrier function in MS and clinically isolated syndrome highlighted(22/09/14)

Microparticles in multiple sclerosis and clinically isolated syndrome: effect on endothelial barrier function.

Cell-derived microparticles are secreted in response to cell damage or dysfunction. Endothelial and platelet dysfunction are thought to contribute to the development of multiple sclerosis (MS).

Our aim here is, first, to compare the presence of microparticles of endothelial and platelet origin in plasma from patients with different clinical forms of MS and with clinically isolated syndrome. Second, to investigate the effect of microparticles on endothelial barrier function.

Results: Platelet-poor plasma from 95 patients (12 with clinically isolated syndrome, 51 relapsing-remitting, 23 secondary progressive, 9 primary progressive) and 49 healthy controls were analyzed for the presence of platelet-derived and endothelium-derived microparticles by flow cytometry.

The plasma concentration of platelet-derived and endothelium-derived microparticles increased in all clinical forms of MS and in clinically isolated syndrome versus controls. The response of endothelial barriers to purified microparticles was measured by electric cell-substrate impedance sensing.

Microparticles from relapsing-remitting MS patients induced, at equivalent concentrations, a stronger disruption of endothelial barriers than those from healthy donors or from patients with clinically isolated syndrome. MS microparticles acted synergistically with the inflammatory mediator thrombin to disrupt the endothelial barrier function.

Conclusions: Plasma microparticles should be considered not only as markers of early stages of MS, but also as pathological factors with the potential to increase endothelial permeability and leukocyte infiltration.

Source: 7thSpace Interactive © 2014 7thSpace Interactive (22/09/14)

Molecule linked to neurological dysfunctions identified(06/08/14)

A team of researchers has pinpointed a small molecule responsible for nerve cell damage and other symptoms tied to neurological diseases, including multiple sclerosis (MS).

In a study published in the June 2014 issue of The Federation of American Societies for Experimental Biology Journal, investigators at The Open University (OU) in the United Kingdom and colleagues from Sheffield, London, and Amsterdam highlighted the behavior of MicroRNA-155 (miR-155) and its activity during inflammation.

According to a statement released by the OU, inflammation in the molecule creates gaps in tissue cells, leading to toxins entering the brain from the bloodstream. In comparison, unaffected individuals’ cells create a barrier that prevents molecules from invading the brain.

“We have identified miR-155 as a critical miRNA in neuroinflammation at the blood-brain barrier (BBB),” the authors noted. “miR-155 is expressed at the neurovascular unit of individuals with MS and of mice with experimental autoimmune encephalomyelitis.”

The statement also noted that cells that line blood vessels and control molecules’ brain access when inflamed become “leaky” due to neurological immunity. This inflammation, the study noted, has been observed with several conditions such as MS, HIV, dementia, and bacterial infections of the blood.

The investigators said that while BBB dysfunction was recognised in MS and stroke patients, molecular activity behind the dysfunction is still a mystery.

"This research has helped us to gain a better understanding of how toxins and other blood-borne molecules are leaked into the brain in inflammatory conditions,” lead author Ignacio Romero, MD, senior lecturer in Cellular Neuroscience in Open University’s Department of Life, Health and Chemical Sciences, said in a statement.“This is crucial, not only for helping to explain the molecular underpinnings of neurological diseases such as Alzheimer’s and MS, but also for opening up new possibilities for developing treatments to reduce the flow of these unwanted molecules to the brain and also for delivering life-saving drugs.”

Source: HCP Live Copyright HCPLive 2006-2014 (06/08/14)