The innate immune system is crucial to our survival, but excessive or persistent proinflammatory cytokine production can result in tissue damage and organ injury, such as in autoimmune diseases. These results could have important implications for the treatment of conditions associated with excessive or persistent inflammation, such as autoimmune diseases. In conclusion, we demonstrate that voluntary activation of the sympathetic nervous system results in epinephrine release and subsequent suppression of the innate immune response in humans in vivo. Finally, flu-like symptoms were lower in the intervention group.
Levels of proinflammatory mediators TNF-α, IL-6, and IL-8 were lower in the intervention group and correlated negatively with IL-10 levels. In the intervention group, plasma levels of the anti-inflammatory cytokine IL-10 increased more rapidly after endotoxin administration, correlated strongly with preceding epinephrine levels, and were higher. In the intervention group, practicing the learned techniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundly increased plasma epinephrine levels. administration of 2 ng/kg Escherichia coli endotoxin). Subsequently, all subjects underwent experimental endotoxemia (i.v. Subjects in the intervention group were trained for 10 d in meditation (third eye meditation), breathing techniques (i.a., cyclic hyperventilation followed by breath retention), and exposure to cold (i.a., immersions in ice cold water). Healthy volunteers were randomized to either the intervention ( n = 12) or control group ( n = 12). Herein, we evaluated the effects of a training program on the autonomic nervous system and innate immune response.
However, both the autonomic nervous system and innate immune system are regarded as systems that cannot be voluntarily influenced. Acute activation of the sympathetic nervous system attenuates the innate immune response. Excessive or persistent proinflammatory cytokine production plays a central role in autoimmune diseases.
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