Depression is a complex, multifactorial disorder with a pathophysiology that is still not fully understood. Recent research suggests that neuroinflammation and disruption of the blood-brain barrier may play a significant role in the development of depressive symptoms. Chemokines, particularly eotaxin-1, have emerged as a key component linking peripheral immune activation to central nervous system changes. Elevated levels of eotaxin-1 have been associated with reduced neurogenesis, cognitive decline, and depression-like behavior. Stress and infections can damage the blood-brain barrier, allowing peripheral chemokines such as eotaxin-1 to enter the brain or be locally expressed, potentially triggering neuroinflammation. Overall, findings suggest that chemokine signaling following blood- brain barrier disruption may play a crucial role in the pathogenesis of depression and could offer potential targets for therapeutic intervention. (Neuropsychopharmacol Hung 2025; 27(2): 115-120)