Inflammatory Markers In Depression

Timothy G. Dinan

Disclosures

Curr Opin Psychiatry. 2009;22(1):32-36. 

In This Article

Cytokines in Depression

Kim et al. [14•] examined the cytokine balance in patients with major depression. They found an activation of monocytic proinflammatory cytokines and inhibition of both Th1 and Th2 cytokines and speculated that TGF-β may play a key role in association with the regulation of monocytic cytokines as well as Th1 and Th2 in depression. We examined proinflammatory and anti-inflammatory cytokine levels in patients who were SSRI resistant.[15•] Patients with SSRI-resistant depression had significantly higher production of the proinflammatory cytokines IL-6 and TNF-α than normal controls. Euthymic patients who were formerly SSRI resistant had proinflammatory cytokine levels that were similar to the healthy individuals group. Anti-inflammatory cytokine levels did not differ across the three groups. The suppression of proinflammatory cytokines does not occur in depressed patients who fail to respond to SSRIs and is necessary for clinical recovery.

Eller et al. [16•] examined the impact of escitalopram on proinflammatory cytokines in major depression. They followed 100 patients through a course of therapy with escitalopram 10-20 mg daily. The main finding was the fact that higher basal levels of TNF-α were associated with nonresponse. A similar study reported the effects of another SSRI, namely sertraline, over 8 weeks of treatment.[17•] At the baseline, proinflammatory cytokines were elevated while anti-inflammatory cytokines were suppressed. Sertraline treatment resulted in a significant decrease in IL-12 and an increase in IL-4 and TGF-β.

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