The inflammatory hypothesis is one of the more widely accepted pathogenesis of depression. Glia plays an important immunomodulatory role in neuroinflammation, mediating interactions between the immune system and the central nervous system (CNS). Glial cell-driven neuroinflammation is not only an important pathological change in depression, but also a potential therapeutic target. This review discusses the association between depression and glial cell-induced neuroinflammation and elucidates the role of glial cell crosstalk in neuroinflammation. Firstly, we focus on the role of glial cells in neuroinflammation in depression and glial cell interactions
secondly, we categorize changes in different glial cells in animal models of depression and depressed patients, focusing on how glial cells mediate inflammatory responses and exacerbate depressive symptoms
Thirdly, we review how conventional and novel antidepressants affect the phenotype and function of glial cells, thereby exerting anti-inflammatory activity
finally, we discuss the role of the gut-brain axis in glial cell function and depression, and objectively analyze the problems that remain in current antidepressant therapy. This review aims to provide an objective analysis of how glial cell cross-talk may mediate neuroinflammation and thereby influence pathologic progression of depression. It is concluded that a novel therapeutic strategy may be to ameliorate glial cell-mediated inflammatory responses.