THE INTERACTION BETWEEN INFLAMMATION AND STRESS IN DEPRESSION

Abstract

While the role of inflammation in depression has been extensively studied over the past few decades, underlying mechanisms are still not well understood and findings remain inconclusive. There is growing evidence that the pathophysiology of depression may be contingent on interactions between pro-inflammatory and anti-inflammatory agents instead of their independent effects. Despite well-established links between pro-inflammatory cytokines and cortisol, however, their interactions have yet to be properly investigated in depression. Disruptions to the homeostatic balance between pro-inflammatory cytokines and cortisol may signal an impaired cytokine-glucocorticoid feedback circuit and an increased vulnerability to depression. Because cortisol can be anti-inflammatory, it may also buffer against the negative effects of pro-inflammatory cytokines. The present study aimed to address this gap by utilizing data from a national mental health study conducted among 11 to 18-year-old Singaporean adolescents. Two hundred and twenty-eight adolescents were included in the investigation. Measures of depression were administered while saliva samples were collected for testing of IL-6 and cortisol. Consistent with our hypothesis, we found a significant interaction effect where IL-6 was negatively associated with depression only under high cortisol but not low cortisol conditions. Our findings provide support for the protective role of cortisol against inflammation in depression.