[Inflammatory depression: a review of advances in pathophysiology, clinical implications, and treatment]

Major depressive disorder (MDD) is a highly prevalent and disabling condition, and although conventional treatments focused on monoaminergic neurotransmission have been helpful for many individuals, a substantial proportion of patients fail to achieve adequate symptom remission. Over the past decade, accumulating evidence has highlighted systemic inflammation as a central component in the pathophysiology of MDD, suggesting that immune dysregulation may characterize a distinct subgroup of patients. Activation of the immune system can adversely influence neurotransmission, impair neuroplasticity, disrupt the hypothalamic-pituitary-adrenal (HPA) axis, and promote glial cell activation, all of which can contribute to chronicity and resistance to standard therapies. This understanding has led to the proposal of "inflammatory depression" as a specific endotype within the broader depressive spectrum. Recognizing this profile is essential for advancing precision medicine and improving clinical decision-making. It is increasingly postulated that these patients may benefit from targeted anti-inflammatory strategies, including pharmacologic agents, nutraceuticals, structured physical exercise, and dietary interventions with immunomodulatory effects. Despite these promising avenues, more rigorous clinical trials are needed to establish standardized protocols and refine patient selection based on inflammatory biomarkers, ensuring more effective and personalized treatment approaches.