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The role of inflammatory cytokines on the aetiopathogenesis of depression

Objective: The primary focus of this review is to provide an overview of the role of inflammation in the development of depression. The article will describe how inflammatory cytokines contribute to depression via action on three major pathways in the brain: the neuroendocrine; neurotransmitter depletion; and neuroprogression pathways. Methods: An online literature search was carried out in July 2012. Original articles and reviews were selected if they discussed the role of inflammation on the development of depression. Results: There is a large body of current research on the role of inflammatory cytokines on the development of depression. Cytokines have been found to interact with different pathways in the brain, and may contribute to the development of depression. Cytokines cause hypercortisolaemia by dysregulation of the hypothalamic–pituitary–adrenal axis directly by activating it and indirectly by modifying glucocorticoid receptor sensitivity to cortisol leading to cortisol hypersecretion. Cytokines deplete central synaptic serotonin levels by reducing its synthesis and increasing its reuptake. They may also deplete neurotrophic factors which are believed to play a neuroprotective role against depression. Cytokines activate cellular cascades that cause excitotoxicity and apoptosis and inhibit neurogenesis in the hippocampus. Conclusion: There is a growing body of correlative studies that suggest inflammatory cytokines may be a central factor that can affect multiple neuronal pathways and have an additive effect on the development of depression. However, the fact that not all people with inflammatory conditions suffer from depression suggests that depression is not purely a result of elevated inflammatory cytokines. Depression may be a result of a complex pathology that remains an area of growing interest and importance.