The influenza virus triggered multiple sclerosis relapses in mice models.
Influenza virus could trigger multiple sclerosis (MS) relapse, having shown to do so in mice models in a recent study.
Researchers from the University of Illinois Urbana-Champaign used mice models of MS in order to investigate how the flu impacts human MS patients. The investigators then exposed the mice to influenza to observe the effects in the mice and on their brains, specifically looking for inflammatory demyelination.
The researchers added that it is well understood that patients with MS are at risk for relapse when they have upper respiratory infections, but the cause for relapse was not known. During this time, they explained, immune cells want to get to the brain.
About a third of the mice showed signs of MS relapse, though influenza was not present in the brains of the mice, the researchers determined. Upon closer inspection, the study authors determined that there was an increase in glial activation in the brains of the influenza infected mice. Study author Andrew Steelman (pictured), PhD, told MD Magazine that this was the team’s most surprising finding.
“Not all of the transgenic mice inoculated with influenza developed disease,” Steelman said. “This was surprising since the overwhelming majority of T cells in this strain are autoreactive. We were also surprised to find trafficking of immune cells (monocytes, neutrophils and T cells) to the brain during peripheral infection in wild-type mice.”
The researchers then theorized that glia might be communicating with immune cells and redirecting them to the brain via molecules called chemokines. Levels of a specific chemokine, CXCL5, were elevated in the brains of the mice infected with the flu. CXCL5 is also elevated in the cerebral spinal fluid in human MS patients when they undergo a relapse. Another group of researchers has recently suggested that monitoring CXCL5 could be used to predict relapse.
“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 two,” Steelman said. “That’s actually the same incidence and timeframe we saw in our infected mice, although we thought it would be much higher given that most of the immune cells in this mouse strain are capable of attacking the brain.”
Steelman noted that their findings right now might not change the way physicians treat their patients, but in the future, moving closer to a drug intervention should be possible after more analysis and observation of the CXCL5 molecule. He explained that once the environmental factors for infection that cause relapse are identified — such as a runny nose of fever – relapses may even be inhibited. He said that if relapses could be cut down by 50 %, in theory, the time it takes for a patient to experience continual loss of function and disability could be prolonged.
The paper, “Influenza infection triggers disease in a genetic model of experimental autoimmune encephalomyelitis,” was published in the Proceedings of the National Academy of Sciences.
A press release regarding the study was made available.