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A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

P-selectin-mediated monocyte-cerebral endothelium adhesive interactions link peripheral organ inflammation to

Charlotte D'Mello1, Kiarash Riazi, Tai Le

  • 1Immunology Research Group and Gastrointestinal Research Group, Calvin, Phoebe, and Joan Snyder Institute for Chronic Diseases, and Hotchkiss Brain Institute, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 13, 2013
PubMed

Insights

Peripheral inflammation triggers monocyte adhesion in the brain, leading to sickness behaviors. This involves TNFα-TNFR1 signaling and P-selectin, impacting neural activity and offering therapeutic targets.

Area of Science:

  • Neuroimmunology
  • Systemic Inflammation Research
  • Cerebral Immune Cell Dynamics

Background:

  • Sickness behaviors (fatigue, mood changes, cognitive dysfunction) are common in systemic inflammation, impacting quality of life.
  • Microglia and cytokines are implicated in central neurotransmission changes, but the link to peripheral inflammation is unclear.

Purpose of the Study:

  • To investigate the connection between peripheral organ inflammation and cerebral immune responses.
  • To elucidate the mechanisms linking peripheral inflammation to sickness behaviors.

Main Methods:

  • Cerebral intravital microscopy in mouse models of liver inflammation and colitis.
  • Analysis of monocyte adhesion to cerebral endothelial cells (CECs).
  • Assessment of TNFα-TNFR1 signaling and P-selectin involvement.

Main Results:

  • Liver inflammation increased monocyte rolling and adhesion along CECs.
  • TNFα-TNFR1 signaling and P-selectin mediated these adhesive interactions.
  • Monocyte-CEC interactions correlated with microglial activation, reduced neural excitability, and sickness behaviors.
  • Similar findings were observed in a colitis model.

Conclusions:

  • Peripheral organ inflammation directly influences cerebral immune cell behavior and neural function.
  • Monocyte adhesion to CECs is a key mechanism linking peripheral inflammation to sickness behaviors.
  • These findings suggest potential therapeutic strategies targeting this pathway for systemic inflammatory diseases.

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