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The immune System and the Role of Inflammation in Perinatal Depression

Neuroscience Bulletin 2016年第4期32卷 398-420页

作者： Philippe Leff-Gelman Ismael Mancilla-Herrera Monica Flores-Ramos Carlos Cruz-Fuentes Juan Pablo Reyes-Grajeda maría del pilar garcía-cuétara Marielle Danitza Bugnot-Perez David Ellioth Pulido-Ascencio National Institute of Perinatology Mexico City Mexico National Institute of Psychiatry Mexico City Mexico National Institute of Genomic Medicine Mexico CityMexico Faculty of Psychology Anahuac University HuixquilucanMexico National Council of Science and Technology Mexico CityMexico

Major depression during pregnancy is a common psychiatric disorder that arises from a complex and mul- tifactorial etiology. Psychosocial stress, sex, hormones, and genetic vulnerability increase the risk for triggering mood disorders. Microglia and toll-like receptor 4 play a crucial role in triggering wide and varied stress-induced responses mediated through activation of the inflammasome; this leads to the secretion of inflammatory cytokines, increased serotonin metabolism, and reduction of neurotransmitter availability along with hypothalamic-pituitary-adrenal axis hyperactivity. Dysregulation of this intricate neu- roimmune communication network during pregnancy modifies the maternal milieu, enhancing the emergence of depressive symptoms and negative obstetric and neu- ropsychiatric outcomes. Although several studies have clearly demonstrated the role of the innate immune system in major depression, it is still unclear how the placenta, the brain, and the monoaminergic and neuroendocrine systems interact during perinatal depression. Thus, in the present review we describe the cellular and molecular interactions between these systems in major depression during preg- nancy, proposing that the same stress-related mechanisms involved in the activation of the NLRP3 inflammasome in microglia and peripheral myeloid cells in depressed patients operate in a similar fashion in the neuroimmune placenta during perinatal depression. Thus, activation of Toll-like receptor 2 and 4 signaling and the NLRP3 inflammasome in placental immune cells may promote a shift of the Thl/Th2 bias towards a predominant Thl/Thl7 inflammatory response, associated with increased secretion of pro-inflammatory cytokines, among other secreted autocrine and paracrine mediators, which play a crucial role in triggering and/or exacerbating depressive symptoms during pregnancy.

关键词： Depression Pregnancy immune systeminflammation Cytokine Serotonin Indoleamine dioxygenase Glucocorticoid Brain Placenta

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