Resulting increase in IL-6 expression creates a proinflammatory environment, interfering with the early immune response to infection.

Social stress raises levels of interleukin-6 (IL-6), which then makes mice vulenerable to multiple sclerosis (MS)-like illnesses, report researchers from Texas A&M University.

The team used a social disruption model to simulate stress in mice and then infected them with Theiler’s murine encephalomyelitis (TMEV). This resulted in an acute infection of the central nervous system followed by a chronic autoimmune disease similar to that seen in humans with MS, the team says.

In one experiment, they found that mice exposed to social disruption had elevated central and peripheral levels of IL-6. Infusing an IL-6-neutralizing antibody into the brain prevented this increase. Results from a second experiment showed that administering the IL-6 neutralizing antibody during the stress exposure prevented worsening of the TMEV infection.

Mary Meagher, Ph.D., lead researcher, proposes that the adverse effects of stress-induced IL-6 on TMEV infection are enough to create a proinflammatory environment that interferes with the immune response to infection. Since the early immune response shapes the later specific reactions to infection, impairment of the initial stage could account for the increased viral level, prolonged viral infection, increased CNS inflammation, and the subsequent exacerbation of the chronic autoimmune disease.

The research was presented at the “115th Annual Convention of the American Psychological Association.”

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