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Decoding microglia responses to psychosocial stress reveals blood-brain barrier breakdown that may drive stress

Michael L Lehmann1, Thaddeus K Weigel2, Hannah A Cooper2

  • 1Section on Functional Neuroanatomy, Intramural Research Program, National Institute of Mental Health, NIH, Bethesda, MD, 20892, USA. michael.lehmann@nih.gov.

Scientific Reports
|July 28, 2018
PubMed

Insights

Chronic psychological stress impacts brain immune responses. Susceptible mice show heightened microglial inflammation, oxidative stress, and vascular leakage, contributing to stress susceptibility.

Area of Science:

  • Neuroscience
  • Immunology
  • Stress Research

Background:

  • Chronic psychological stress significantly impacts brain function and behavior.
  • Microglia, the brain's resident immune cells, play a crucial role in neuroinflammation.
  • Individual differences in stress coping mechanisms are not fully understood at the cellular level.

Purpose of the Study:

  • To investigate the role of microglial immune responses in stress susceptibility.
  • To identify molecular pathways in microglia associated with chronic social defeat stress.
  • To explore the link between microglial activity and brain vascular integrity.

Main Methods:

  • Mice were subjected to chronic social defeat (CSD) and categorized as susceptible (CSD-S) or resilient (CSD-R).
  • Microglia were isolated from CSD-S, CSD-R, and control mice for transcriptome analysis (microarray).
  • Histochemical techniques were used to validate array predictions and assess brain vascular leakage.

Main Results:

  • Microglia from CSD-S mice exhibited transcriptomic enrichment in inflammation, phagocytosis, oxidative stress, and extracellular matrix remodeling pathways.
  • CSD-S microglia demonstrated elevated phagocytic activity and increased oxidative stress markers.
  • CSD-S mice, but not CSD-R or controls, showed evidence of brain vascular leakage.

Conclusions:

  • The inflammatory profile of microglia in stress-susceptible individuals may be driven by extracellular matrix degradation, oxidative stress, and microbleeds.
  • Phagocytosis of blood-borne substances entering the brain parenchyma contributes to neuroinflammation in stress susceptibility.
  • These CNS-centric microglial responses are hypothesized to underlie the behavioral phenotype of stress susceptibility.

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