Aug. 19 : A new research has shown that chronic stress can intensify inflammation, and increase the risk of infections in the central nervous system, of neurodegenerative diseases like multiple sclerosis and of other inflammatory diseases.

Researchers from Texas A & M University claim that their study has for the first time demonstrated that stress-related increases in central nervous system inflammation are behind the adverse effects of stress in an animal model of MS.

The researchers used mice to show what role social stress plays in the immune process to influence the course of an MS-like disease. They proposed that stress-induced increases of pro-inflammatory cytokines, which are proteins that regulate immune and inflammatory functions, inhibit the clearing of a virus and allow the inflammatory process to run amok.

According to the study’s authors, stress may interact with viral infections to increase vulnerability to diseases such as MS. They say that meta-analysis of studies investigating the impact of stressful events in patients with MS show an increased risk of worsening symptoms of the disease.

Experiments on mice showed that increases in a particular cytokine called interleukin-6 (IL-6), which is released during stress and regulates the part of the immune system that fights infection, can make socially stressed animals vulnerable to MS-like illnesses.

The study, presented at the 115th Annual Convention of the American Psychological Association (APA), showed that stress elevates levels of IL-6, which subsequently raises the severity of the MS-like illness.

The authors say that using specific IL-6 neutralizing antibody treatments during the stress exposure can prevent the stress-related worsening of the disease.

The researchers say that IL-6 neutralizing antibody may also be helpful in preventing worsening of the Theiler’s murine encephalomyelitis (TMEV) infection, which results in an acute infection of the central nervous system followed by a chronic autoimmune disease similar to that seen in humans with MS.

Based on the new findings, lead researcher Dr. Mary Meagher proposes that the adverse effects of stress-induced IL-6 on TMEV infection are enough to create a pro-inflammatory environment that interferes with the immune response to infection.

Since the early immune response shapes the later specific immune response to infection, its impairment may account for the increased viral level, prolonged viral infection, increased CNS inflammation, and the subsequent exacerbation of the chronic autoimmune disease.

The researchers believe that their findings may help them unravel which bio-behavioural mechanisms offset the adverse health effects of chronic social stress in humans.

“Similar to mice exposed to repeated social defeat by an aggressive intruder, people exposed to chronic social conflict experience high levels of stress and consequent dysregulation of the immune system, thereby increasing vulnerability to infectious and autoimmune disease,” said Meagher.

“The cytokine response during chronic stress appears to play a key role in exacerbating the acute CNS infection and the development of subsequent autoimmune responses,” Meagher added.

The researcher further said that interventions that prevented or reversed the stress-induced increases in IL-6 in the mouse model may have implications for humans, but admits that human clinical trials are needed to fully evaluate this issue. (ANI)