Science News, March 27, 1999 People who feel unable to deal with life’s stresses display an exaggerated immune reaction that may intensify their sneezing, soughing, and other physical symptoms once they ” ve contracted a common virus, a new study suggests. However, the researchers have not yet confirmed whether this particular immune response-a sharp rise in the production of a chemical messenger known as interleukin-6 (IL-6) -magnifies cold like respiratory symptoms or occurs in response to them. Sheldon Cohen of Carnegie Mellon University says this is the first linkage of psychological stress to an immune system change. Cohen and his colleagues previously found that high levels of mental stress increase the risk of becoming infected by respiratory viruses and developing cold symptoms. Participants in the research were chosen by a newspaper ad, and then were quarantined in separate rooms of a hotel for eight days. On the first day, they underwent physical examinations and were tested for viral infections.
The next day, each volunteer received nasal drops containing an infectious dose of an influenza A virus. The researchers verified that all the volunteers developed infections from the virus during their hotel stays. At the end of each day, participants rated the severity of the cold symptoms. These consisted of sneezing, nasal congestion and discharge, sore throat, cough, headache, chilliness, and feeling uneasy and uncomfortable. Mucus production was assessed by gathering it in a plastic bag. IL-6 levels were taken from the discharged mucus.
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Those individuals reporting high levels of stress in their lives produced the most mucus, displayed the largest surges in IL-6 production, and cited the most-severe symptoms of respiratory infection during the course of the study. When a virus infringes on a cell’s ability to function, IL-6 release attracts immune cells to that site. In the case of a respiratory infection, IL-6 production ignites a process that results in cold symptoms. Psychological stress may loosen physiological controls on IL-6 release, leading to its overproduction in the face of viral infection.
It’s also possible that the increase in IL-6 for stressed people reflects a larger and much more complex immune process triggered during the course of viral infections. However, Il-6 may react with great sensitivity to psychological stress without serving as a physiological bridge to cold symptoms. In a follow up investigation, Cohen’s group plans to stimulate IL-6 release in immune cells grown in the laboratory. The researchers will then see if the individuals who provided the cells generating the highest concentrations of IL-6 also experienced the greatest stress and respond to virus with severe cold symptoms.
They are no drugs available to block the impact of IL-6 yet.
