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Related Experiment Video

Updated: May 30, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

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MMP9 deficiency does not decrease blood-brain barrier disruption, but increases astrocyte MMP3 expression during

Carine Savarin¹, Stephen A Stohlman, Anna M Rietsch

¹Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA.

|July 30, 2011

Summary

This summary is machine-generated.

Neutrophil matrix metalloproteinase-9 (MMP9) is not essential for blood-brain barrier disruption in viral encephalomyelitis. Astrocytes upregulate MMP3 in MMP9-deficient mice, suggesting collaborative roles in regulating brain inflammation.

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Area of Science:

Neuroimmunology
Molecular Biology
Virology

Background:

Matrix metalloproteinases (MMPs), particularly MMP9, are linked to blood-brain barrier (BBB) disruption in neuroinflammatory conditions.
During JHMV infection, MMP9 activity is primarily observed in neutrophils, suggesting a role in leukocyte infiltration.

Purpose of the Study:

To investigate the necessity of MMP9 in BBB disruption and leukocyte infiltration during JHMV-induced encephalomyelitis.
To explore the compensatory roles of other MMPs, like MMP3, in the absence of MMP9.

Main Methods:

Utilized JHMV-infected MMP9-deficient (MMP9(-/-)) and wild-type (WT) mice.
Assessed leukocyte infiltration, BBB integrity, and MMP expression patterns (MMP3, MMP9) in the central nervous system (CNS).
Investigated the impact of neutrophil depletion on CNS leukocyte accumulation.

Main Results:

MMP9 deficiency did not alter BBB disruption or CNS leukocyte infiltration in JHMV-infected mice compared to WT.
Neutrophil depletion reduced monocyte and T cell accumulation but did not affect overall pathogenesis.
MMP9 deficiency led to increased MMP3 expression in astrocytes, suggesting a compensatory mechanism.

Conclusions:

Neutrophil-derived MMP9 is not the sole mediator of BBB disruption and leukocyte entry into the CNS during viral encephalomyelitis.
Astrocytes play a significant role in regulating BBB permeability, potentially collaborating with infiltrating immune cells.
Targeting individual MMPs for therapeutic intervention in neuroinflammation may be complex due to compensatory mechanisms.