Stroke's Stress Response Weakens Immune System, Increases Infection Risk

A new University of Manchester and Edinburgh study published in the journal Brain, Behavior and Immunity has found that people who have had a stroke have fewer of a specific type of immune cell called B cells, which normally produce antibodies to fight off infections. Surprisingly, the same compromising immune changes were seen when healthy B cells were exposed to norepinephrine—a chemical released by the body after stroke, but also during stress, illness, or intense physical activity. People who have had a stroke are more likely to develop infections such as pneumonia. These infections can slow recovery and make brain injury worse. Understanding why the immune system becomes weaker after stroke could help doctors prevent these infections and improve patient outcomes. Earlier studies by Dr. Laura McCulloch and Dr. Barry McColl at the University of Edinburgh found that in animal models, stroke activates the system behind the fight-or-flight response, which includes the release of the chemical norepinephrine. This activation quickly impairs a group of immune cells called B cells, reducing their ability to produce protective antibodies, and was associated with vulnerability to infection. Until now, it was unclear whether the same thing happens in stroke patients. In this study, carried out at the University of Manchester in collaboration with the University of Edinburgh team, researchers analyzed blood samples from patients 24–48 hours after an ischemic stroke and compared them with samples from individuals who had not had a stroke ('controls'). They found that stroke patients had fewer B cells than control patients and that these remaining cells were also less effective at producing antibodies and special signaling proteins called cytokines, both of which are essential for fighting infections. "Findings from this collaborative study confirm that after someone has had a stroke important immune cells that help to fight infection are reduced, limiting the patient's ability to make protective antibodies. Revealing these changes opens opportunities to develop new treatments that could help reduce the incidence of infection after stroke," said Clinical Study Lead Prof Craig Smith from The University of Manchester. The teams also tested B cells from healthy volunteers. When these cells were exposed to norepinephrine, they showed the same responses as seen in stroke patients: increased cell death and reduced antibody production. These findings suggest that activation of the fight-or-flight response itself, not just stroke, can impair immune function. Stress, illness, or extreme physical exertion may all influence how well B cells work. Reduced numbers of immune cells (B cells) were found in the blood of patients 24–48 hours after an ischemic stroke. When B cells were stimulated with bacterial proteins (mimicking an infection), they were less able to produce protective antibodies and signaling proteins called cytokines. The researchers are now studying how these immune changes after stroke may affect long-term recovery, including thinking and memory, as well as further damage to the brain's blood vessels. They are also exploring new treatments aimed at protecting or restoring B cell function after stroke, with the goal of reducing infections and improving recovery.