Open Access

Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review

  • Authors:
    • Előd Ernő Nagy
    • Attila Frigy
    • József Attila Szász
    • Emőke Horváth
  • View Affiliations

  • Published online on: June 24, 2020     https://doi.org/10.3892/etm.2020.8933
  • Pages: 2510-2523
  • Copyright: © Nagy et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Increasing evidence hints to the central role of neuroinflammation in the development of post‑stroke depression. Danger signals released in the acute phase of ischemia trigger microglial activation, along with the infiltration of neutrophils and macrophages. The increased secretion of proinflammatory cytokines interleukin (IL)‑1β, IL‑6, IL‑8, and tumor necrosis factor α (TNFα) provokes neuronal degeneration and apoptosis, whereas IL‑6, interferon γ (IFNγ), and TNFα induce aberrant tryptophane degradation with the accumulation of the end‑product quinolinic acid in resident glial cells. This promotes glutamate excitotoxicity via hyperexcitation of N‑methyl‑D‑aspartate receptors and antagonizes 5‑hydroxy‑tryptamine, reducing synaptic plasticity and neuronal survival, thus favoring depression. In the post‑stroke period, CX3CL1 and the CD200‑CD200R interaction mediates the activation of glial cells, whereas CCL‑2 attracts infiltrating macrophages. CD206 positive cells grant the removal of excessive danger signals; the high number of regulatory T cells, IL‑4, IL‑10, transforming growth factor β (TGFβ), and intracellular signaling via cAMP response element‑binding protein (CREB) support the M2 type differentiation. In favorable conditions, these cells may exert efficient clearance, mediate tissue repair, and might be essential players in the downregulation of molecular pathways that promote post‑stroke depression.

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September-2020
Volume 20 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Nagy EE, Frigy A, Szász JA and Horváth E: Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review. Exp Ther Med 20: 2510-2523, 2020
APA
Nagy, E.E., Frigy, A., Szász, J.A., & Horváth, E. (2020). Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review. Experimental and Therapeutic Medicine, 20, 2510-2523. https://doi.org/10.3892/etm.2020.8933
MLA
Nagy, E. E., Frigy, A., Szász, J. A., Horváth, E."Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review". Experimental and Therapeutic Medicine 20.3 (2020): 2510-2523.
Chicago
Nagy, E. E., Frigy, A., Szász, J. A., Horváth, E."Neuroinflammation and microglia/macrophage phenotype modulate the molecular background of post-stroke depression: A literature review". Experimental and Therapeutic Medicine 20, no. 3 (2020): 2510-2523. https://doi.org/10.3892/etm.2020.8933