August 23, 2017
When people with multiple sclerosis (MS) get the flu, they are at increased risk of an MS relapse. A recent study designed to investigate this flu-relapse link suggests exposure to an upper respiratory virus causes glial activation, which in turn promotes immune cell trafficking to the central nervous system (doi: 10.1073/pnas.1620415114).
The study, published in the Proceedings of the National Academy of Sciences, involved laboratory mice genetically prone to developing an autoimmune attack of the brain and spinal cord. After exposure to influenza, some of the mice went on to experience MS-like symptoms, researchers found, even when the virus was not found in the brain.
“If you look at a population of MS patients that have symptoms of upper respiratory disease, between 27% and 42% will relapse within the first week or 2,” said researcher Andrew Steelman, PhD, an assistant professor at the University of Illinois, in a university press release (August 8, 2017). “That’s actually the same incidence and timeframe we saw in our infected mice.”
In the brains of flu-infected mice, researchers identified an increase in glial activation.
“When glia become activated, you start to see trafficking of immune cells from the blood to the brain. We think that, at least for MS patients, when glia become activated, this is 1 of the initial triggers that causes immune cells to traffic to the brain,” Dr Steelman said. “Once there, the immune cells attack myelin, the fatty sheaths surrounding axons, causing neurologic dysfunction.”
Researchers suspect glia may use chemokines to signal immune cells. A specific chemokine, CXCL5, was elevated in the brains of flu-infected mice — and in the cerebral spinal fluid of humans experiencing MS relapse, they reported. Other investigators have recently suggested CXCL5 could be used to predict relapse, strengthening Dr Steelman’s confidence in his team’s finding.
As to why the immune system attacks the brain during upper respiratory infection, researchers are still not sure.
“MS patients have 1or 2 relapses a year. It’s thought that these relapses contribute to the progression of the disease,” Dr Steelman said. “If we can pinpoint what’s driving environmental factors such as infection to cause relapse, then maybe we can intervene when the patient has signs of sickness, like runny nose or fever. If we could inhibit relapse by 50%, we could theoretically prolong the time it takes for the patient to experience continual loss of function and dramatic disability.”