A new study has indicated that stress- related inflammation might lead to an increase in the risk of depression.
The study conducted at the Icahn School of Medicine at Mount Sinai showed that preexisting differences in the sensitivity of a key part of each individual's immune system to stress confer a greater risk of developing stress-related depression or anxiety.
The new study measured the cytokine IL-6 in non-aggressive mice prior to and after repeated social stress invoked by an aggressive mouse. They found that IL-6 levels were higher in mice that were more susceptible to stress than in "stress-resilient" mice. They also found the levels of leukocytes (white blood cells that release IL-6) were higher in stress susceptible mice before stress exposure. The researchers then validated the increased levels of IL-6 in two separate groups of human patients diagnosed with treatment-resistant Major Depressive Disorder.
Lead author Georgia Hodes, PhD, Postdoctoral Researcher in Neuroscience, said that their data suggested that pre-existing individual differences in the peripheral immune system predicted and promoted stress susceptibility.
Hodes added that they found that when mice were given bone marrow transplants of stem cells that produce leukocytes lacking IL-6 or when injected with antibodies that block IL-6 prior to stress exposure, the development of social avoidance was reduced compared with their respective control groups, demonstrating that the emotional response to stress can be generated or blocked in the periphery.
The new study provides experimental evidence that the emotional response to stress can be generated or blocked in the periphery, offering the potential for new forms of treatment for stress disorders and may eventually inform therapeutic strategies to reengineer a patient's immune system to reduce stress vulnerability.
The study is published in the Proceedings of the National Academy of Sciences (PNAS).
