Depression and inflammation: Pathophysiology and therapeutic implications

Depression may result in far reaching adverse health outcomes in addition to impaired sociooccupational or quality of life. Depression is commonly associated with greater cardiovascular morbidity and mortality. Dysregulated inflammation has been suggested as one of the plausible underlying mechanism relating the two. Several studies have reported elevated levels of proinflammatory cytokines and acute phase proteins in depression patients. The proinflammatory cytokines have been shown to alter various signaling pathway relevant to depression such as neurotransmitter metabolism, neuroendocrine dysfunction, and synaptic plasticity after reaching the brain. Potential pathways which have been implicated in mediating the depression and inflammation include the tryptophan-kynurenine pathway, hypothalamic-pituitary-adrenal axis dysregulation, and neuronal plasticity. Inflammation appears to play a pivotal role in the pathophysiology of depression but only in subset of depressive patients. It may prove to be an effective target to develop several treatment modalities and thus open avenues for development of potential therapeutic strategies in vulnerable at risk depressive patients

A study of changes in inflammatory markers in patients of depression

Background: Depression may result in unfavorable health outcomes as it has been associated with cardiovascular morbidity. Recent researches have suggested the role of inflammation in the pathophysiology of depression and co-morbidities associated with it although the underlying mechanism relating the two is still unclear. Aim: The present study aimed to explore the association between depression and inflammatory markers including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and high sensitive c-reactive protein (hsCRP). Materials and Methods: Thirty drug-naοve patients of depression diagnosed on the basis of ICD-10 criteria, in the age group of 20-45 years were included in the study. They were compared with 30 age, gender, body mass index, socio-economic and educational status matched apparently healthy controls. The blood samples were taken after an overnight fast and serum samples were immediately stored until the time of analysis. Results: The serum levels of hsCRP were significantly higher (P = 0.042) in depression group as compared to the control group. Although the mean serum levels of IL-6 and TNF-α were higher in patients of depression, they were not statistically significant (IL-6: P = 0.055, TNF-α: P = 0.053). Conclusion: It can be inferred from our study that depression is associated with underlying low-grade inflammation, which might contribute to increased morbidity in patients of depression