Related Experiment Video
Updated: Jun 27, 2026
Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats
Published on: October 17, 2018
Microglial activation and intracerebral hemorrhage
1Department of Pharmacological Sciences, Stony Brook University, Stony Brook, New York 11794-8651, USA.
Introduction:
Microglia activate upon injury, migrate to the injury site, proliferate locally, undergo morphological and gene expression changes, and phagocytose injured and dying cells. Cytokines and proteases secreted by these cells contribute to the injury and edema formed. We studied the injury outcome after local elimination/paralysis of microglia.
Methods:
Adult male mice were subjected to intracerebral hemorrhage (ICH) by intra-caudate injection of either collagenase or autologous blood. Mice survived for different periods of time, and were subsequently evaluated for neurological deficits, size of the hematoma, and microglia activation. Mice expressing an fms-GFP transgene or the CD11b-HSVTK transgene were also used. For elimination of monocytes/macrophages, CD11b-HSVTK mice were treated with ganciclovir prior to hemorrhage. Modifiers of microglial activation were also used.
Results:
Induction of ICH resulted in robust microglia activation and recruitment of macrophages. Inactivation of these cells, genetically or pharmacologically, pointed to a critical role of the time of such inactivation, indicating that their role is distinct at different time points following injury. Edema formation is decreased when microglia activation is inhibited, and neurological outcomes are improved.
Conclusions:
Microglia, as immunomodulatory cells, have the ability to modify the final presentation of ICH.
Insights
Inhibiting microglia activation after intracerebral hemorrhage (ICH) reduces brain edema and improves neurological outcomes. The timing of microglia inactivation is critical for modifying ICH outcomes.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are key immune cells in the brain that activate, proliferate, and migrate to injury sites following central nervous system damage.
- Activated microglia release cytokines and proteases, contributing to secondary injury and edema formation after events like intracerebral hemorrhage (ICH).
Purpose of the Study:
- To investigate the role of microglia in the outcome of intracerebral hemorrhage (ICH).
- To determine the effect of local microglia elimination or paralysis on injury progression and neurological deficits following ICH.
Main Methods:
- Adult male mice underwent intracerebral hemorrhage (ICH) induced by collagenase or autologous blood injection.
- Microglia and macrophage activity was modulated using genetic approaches (fms-GFP, CD11b-HSVTK transgenes, ganciclovir treatment) and pharmacological agents.
- Neurological deficits, hematoma volume, and microglia activation were assessed at various time points post-ICH.
Main Results:
- ICH robustly activated microglia and recruited macrophages to the injury site.
- Inactivating microglia/macrophages at specific times post-ICH demonstrated their distinct roles in injury progression.
- Inhibition of microglia activation led to decreased edema formation and improved neurological outcomes.
Conclusions:
- Microglia act as crucial immunomodulatory cells that significantly influence the final outcome of intracerebral hemorrhage.
- Targeting microglia activation represents a potential therapeutic strategy for mitigating brain damage after ICH.
More Related Videos
Related Concept Videos
01:29Hemorrhagic Stroke ll: Pathophysiology
01:17Hemorrhagic Stroke l: Introduction
01:26Bacterial Meningitis II: Pathophysiology