Peripheral blood inflammatory markers in depression: Response to electroconvulsive therapy and relationship with cognitive performance

The inflammatory response may play a role in depression and the response to antidepressants. Electroconvulsive therapy (ECT), the most acutely powerful antidepressant treatment, can also affect the innate immune system. Here, we determined circulating blood concentrations of the inflammatory mediators C-reactive protein (CRP), IL-10, IL-6, IL-10, and TNF-alpha in depressed patients compared to healthy controls and assessed the effect of ECT on their concentrations. Relationships between inflammatory mediator concentrations and mood/cognition scores were also explored. Plasma CRP, IL-10, IL-6, IL-10, and TNF-alpha concentrations were examined in 86 depressed patients and 57 controls. Relationships between inflammatory mediators and clinical or cognitive outcomes following ECT were assessed using correlation and linear regression analyzes, respectively. CRP, IL-6, IL-10, and TNF-alpha were elevated in patients at baseline/pre-ECT compared to controls. However, only IL-6 and TNF-alpha sur-vived adjustment for potential confounders. IL-10 was undetectable in most samples. ECT did not significantly alter plasma concentrations of any of the inflammatory mediators. No relationship was identified between CRP, IL-6, IL-10, and TNF-alpha and mood or neurocognitive scores. Overall, our data do not support a major role for these four inflammatory markers in clinical outcomes following ECT or in cognition.

Automated summary

The inflammatory response and its effect on depression and antidepressant treatment, including electroconvulsive therapy (ECT), were examined. The study found elevated levels of certain inflammatory markers in depressed patients compared to healthy controls, but these markers did not show a significant relationship with mood or neurocognitive outcomes. ECT did not alter the concentrations of these inflammatory mediators. The findings suggest that these specific inflammatory markers may not play a major role in clinical outcomes following ECT.