It turns out that stress taps into this very same circuit, but starting in the brain rather than the immune system. Maier and his colleagues find that if they stress animals--by socially isolating them or giving them electrical shock--they see massive increases in interleukin-1 in the hippocampus.
"Stress and infection activate overlapping neural circuits that critically involve interleukin-1 as a mediator," said Maier.
And, not only does stress produce the expected stress response, it also produces exactly the same behavioral changes--including decreased food and water intake and decreased exploration--and physiological changes, including fever, increased white blood cell count and activated macrophages seen in the "sickness response."
"These animals are physically sick after stress," said Maier. "You see everything you see with infection."
The implications of this shared neural loop are that stress and infection sensitize the body's reaction to the other. In other words, an infection primes the circuit so that it has an exaggerated response to later stress and vice versa.
"How you react to a stressor or an infectious agent depends critically on events of the other type in the past," said Maier. And, he added, the effect isn't short-lived. He's measured it out to 10 days.
And so it appears that stress enhances immunity--at least the nonspecific, first-line immunity, said Maier, which makes some evolutionary sense. If we're under stress-- about to be attacked by a wild animal, for example--we would want to prime our first-line immune response to be ready in case of injury.
"Stress is another form of infection," he said. "And the consequences of stress are mediated by the activation of circuits that actually evolved to defend against infection."
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