BY BRUCE GOLDMAN
Firdaus Dhabhar
A study spearheaded by a Stanford University School of Medicine scientist has tracked the trajectories of key immune cells in response to short-term stress and traced, in great detail, how hormones triggered by such stress enhance immune readiness. The study, conducted in rats, adds weight to evidence that immune responsiveness is heightened, rather than suppressed as many believe, by the so-called “fight-or-flight” response.
The study’s findings provide
a thorough overview of how a triad of stress hormones affects the main cell subpopulations of the immune system. They also offer the prospect of, someday, being able to manipulate stress-hormone levels to improve patients’ recovery from surgery or wounds or their responses to vaccines.
You’ve heard it a thousand times: Stress is bad for you. And it’s certainly true that chronic stress, lasting weeks and months, has deleterious effects including, notably, suppression of the immune response. But
short-term stress — the fight-or-flight response, a mobilization of bodily resources lasting minutes or hours in response to immediate threats — stimulates immune activity, said lead author Firdaus Dhabhar, PhD, an associate professor of psychiatry and behavioral sciences and a member of the Stanford Institute for Immunity,
And that’s a good thing.
The immune system is crucial for wound healing and preventing or fighting infection, and both wounds and infections are common risks during chases, escapes and combat.
Working with colleagues at Stanford and two other universities in a study published online June 22 in Psychoneuroendocrinology, Dhabhar showed that
subjecting laboratory rats to mild stress caused a massive mobilization of several key types of immune cells into the bloodstream and then onto destinations including the skin and other tissues. This large-scale migration of immune cells, which took place over a time course of two hours, was comparable to the mustering of troops in a crisis, Dhabhar said. He and colleagues had previously shown that a similar
immune-cell redistribution in patients experiencing the short-term stress of surgery predicts enhanced postoperative recovery.
In the new study, the
investigators were able to show that the massive redistribution of immune cells throughout the body was orchestrated by three hormones released by the adrenal glands, in different amounts and at different times, in response to the stress-inducing event. These hormones are the brain’s call-to-arms to the rest of the body, Dhabhar said.
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Stanford study explains how stress can boost immune system - Office of Communications & Public Affairs - Stanford University School of Medicine
