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Updated: Dec 30, 2025
Author Spotlight: Investigating the Complex Immune Response Following Brain Ischemia
Published on: July 26, 2024
Spleen associated immune-response mediates brain-heart interaction after intracerebral hemorrhage
Wei Li1, Linlin Li2, Wenkui Li2
1Department of Neurology, Henry Ford Hospital, Detroit, MI 48202, USA.
Insights
Splenectomy improved outcomes after intracerebral hemorrhage (ICH) in mice by reducing cardiac dysfunction and cognitive deficits. This suggests the spleen plays a key role in the immune response following ICH, impacting both brain and heart health.
Area of Science:
- Neuroscience
- Cardiology
- Immunology
Background:
- Intracerebral hemorrhage (ICH) often leads to cardiovascular complications, increasing mortality.
- ICH triggers systemic oxidative stress and immune responses, contributing to cardiac dysfunction and heart failure.
- Previous research indicated ICH causes progressive cardiac dysfunction in mice without pre-existing heart conditions.
Purpose of the Study:
- To investigate the role of the immune response in mediating cardiac dysfunction post-ICH.
- To determine if spleen removal (splenectomy) affects neurological and cardiac outcomes after ICH.
Main Methods:
- Adult male mice underwent sham surgery, ICH, or ICH with splenectomy.
- Echocardiography assessed cardiac function at 7 and 28 days post-ICH.
- Neurological and cognitive tests, flow cytometry, western blot, and immunostaining were employed.
Main Results:
- Splenectomy alone did not cause cardiac dysfunction.
- ICH induced significant neurological, cognitive, and cardiac deficits.
- Splenectomy attenuated neurological, cognitive, and cardiac dysfunction post-ICH, reducing cardiac fibrosis and inflammation.
Conclusions:
- Splenectomy mitigates neurological and cardiac dysfunction following ICH in mice.
- Spleen-mediated immune responses and inflammatory cell infiltration contribute to cardiac dysfunction and remodeling after ICH.
Background And Purpose:
Intracerebral hemorrhage (ICH) patients frequently encounter cardiovascular complications which may contribute to increased mortality and poor long term outcome. ICH induces systemic oxidative stress and activates peripheral immune responses which are involved in the pathological cascade leading to cardiac dysfunction and heart failure after ICH. We have previously reported that ICH induces progressive cardiac dysfunction in mice without primary cardiac diseases. In this study, we have investigated the role of immune response in mediating cardiac dysfunction post ICH in mice.
Methods:
Adult male C57BL/6 J mice were randomly assigned to the following groups (n = 8/group): 1) sham control; 2) ICH; 3) splenectomy with ICH (ICH + Spx); 4) splenectomy alone (Spx). Echocardiography was performed at 7 and 28 days after ICH. A battery of neurological and cognitive tests were performed. Flow cytometry, western blot and immunostaining were used to test mechanisms of ICH induced cardiac dysfunction.
Results:
Compared to sham control mice, Spx alone does not induce acute (7 day) or chronic (28 day) cardiac dysfunction. ICH induces significant neurological and cognitive deficits, as well as acute and chronic cardiac dysfunction compared to sham control mice. Mice subjected to ICH + Spx exhibit significantly improved neurological and cognitive function compared to ICH mice. Mice with ICH + Spx also exhibit significantly improved acute and chronic cardiac function compared to ICH mice indicated by increased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), decreased cardiac fibrosis, decreased cardiomyocyte hypertrophy, decreased cardiac infiltration of immune cells and decreased expression of inflammatory factor and oxidative stress in the heart.
Conclusions:
Our study demonstrates that splenectomy attenuates ICH-induced neurological and cognitive impairment as well as ICH-induced cardiac dysfunction in mice. Inflammatory cell infiltration into heart and immune responses mediated by the spleen may contribute to ICH-induce acute and chronic cardiac dysfunction and pathological cardiac remodeling.
