The study, published online in the Journal of Psychoneuroendocrinology and conducted by researchers from the Stanford University School of Medicine and two other universities, adds weight to evidence that immune responsiveness is heightened by the so-called "fight or flight" response.
According to the researchers, their findings offer the prospect of, someday, being able to manipulate stress-hormone levels to improve patients' responses to vaccines or recovery from surgery or wounds.
Chronic stress has detrimental effects including suppression of the immune response. However, lead author of the study Firdaus Dhabhar, Ph.D., an associate professor of psychiatry and behavioral sciences and member of the Stanford Institute for Immunity, Transplantation, and Infection, explained that short-term stress stimulates immune activity.
The immune system plays a vital role in protecting our bodies against diseases, fighting infection and in healing wounds.
Dhabhar explained: "Mother Nature gave us the fight-or-flight stress response to help us, not to kill us."
According to the researchers, the findings describe the body's finely coordinated system to detect danger and prepare to protect itself. Dhabhar said:
"You don't want to keep your immune system on high alert at all times. So nature uses the brain, the organ most capable of detecting an approaching challenge, to signal that detection to the rest of the body by directing the release of stress hormones. Without them, a lion couldn't kill, and an impala couldn't escape."
In the study, the researchers subjected rats to mild stress by confining them (gently, and with full ventilation) in transparent Plexiglas enclosures. The team drew blood several times over a two-hour period and discovered that the stress caused a massive mobilization of several key types of immune cells into the bloodstream and other parts of the body.
In addition, the team found that this mobilization of immune cells was orchestrated by three hormones - norepinephrine, epinephrine and corticosterone - released by the adrenal glands in response to the mild stress.
The hormone cycles worked to bring immune cells out of the spleen and bone marrow into the blood and, finally, to various, "front line" organs.
In order to demonstrate that specific hormones were responsible for movements of specific cell types, the researchers administered the three hormones, separately or in various combinations, to rats whose adrenal glads had been removed so they were unable to produce their own stress hormones.
When the team copied the pattern of stress-hormone release previously seen in the rats, the same immune-cell migration patterns emerged in the rats without adrenal glands. Placebo treatment produced no such effect.
According to Dhabhar, norepinephrine is released early and plays a key role in transporting immune-cell types, such as lymphocytes, monocytes, and neutrophils, into the blood. Furthermore, Epinephrine, transported monocytes and neutrophils into the blood and forced lymphocytes out into destinations such as the skin. Corticosterone, which is released a little later, caused virtually all immune cell types to head out of circulation to destinations such as the skin.
The researchers explained that the overall effect of these movements is to boost immune readiness.
The findings from this study could lead to medical applications, such as administering low doses of stress hormones or drugs that mirror or antagonize them in order to optimize patients' immune readiness for procedures such as surgery or vaccination.
Dhabhar concluded: "More studies will be required including in human subjects, which we hope to conduct, before these applications can be attempted."
Written by Grace Rattue