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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
CCL2 and CCL5 mediate leukocyte adhesion in experimental autoimmune encephalomyelitis--an intravital microscopy study
Adriana Carvalho dos Santos1, Michele Mendes Barsante, Rosa Maria Esteves Arantes
1Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Abstract:
Experimental autoimmune encephalomyelitis (EAE) models multiple sclerosis (MS) and is characterized by marked mononuclear cell influx in the brain. Several studies have demonstrated a role for chemokines during EAE. It remains to be determined whether these mediators modulate EAE primarily by mediating leukocyte influx into the CNS or by modifying lymphocyte activation and/or trafficking into lymphoid organs. After induction of EAE with MOG(35-55), leukocyte recruitment peaked on day 14 and correlated with symptom onset, TNF-alpha production and production of CCL2 and CCL5. Levels of CXCL-10 and CCL3 were not different from control animals. Using intravital microscopy, we demonstrated that leukocyte rolling and adhesion also peaked at day 14. Treatment with anti-CCL2 or anti-CCL5 antibodies just prior to the intravital microscopy prevented leukocyte adhesion, but not rolling. Our data suggest that induction of leukocyte adhesion to the brain microvasculature is an important mechanism by which CCL2 and CCL5 participate in the pathophysiology of EAE.
Insights
Chemokines CCL2 and CCL5 are crucial in experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis model. They promote leukocyte adhesion in the brain, contributing to disease pathology.
Area of Science:
- Neuroimmunology
- Inflammation research
Background:
- Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis (MS).
- Chemokines are implicated in EAE pathogenesis, but their precise roles in leukocyte trafficking versus activation remain unclear.
- Understanding chemokine function is vital for developing targeted MS therapies.
Purpose of the Study:
- To investigate the specific roles of chemokines CCL2 and CCL5 in leukocyte recruitment during EAE.
- To determine if these chemokines mediate leukocyte influx into the central nervous system (CNS) or influence lymphocyte trafficking in lymphoid organs.
Main Methods:
- Induction of EAE using MOG(35-55) peptide.
- Monitoring of leukocyte recruitment, symptom onset, and chemokine production (CCL2, CCL5, CXCL-10, CCL3, TNF-alpha).
- Intravital microscopy to visualize leukocyte rolling and adhesion in brain vasculature.
- Treatment with anti-CCL2 or anti-CCL5 antibodies to assess their impact on leukocyte adhesion.
Main Results:
- Leukocyte recruitment and EAE symptoms peaked around day 14, correlating with CCL2 and CCL5 production.
- Intravital microscopy revealed peak leukocyte rolling and adhesion at day 14.
- Antibody blockade of CCL2 or CCL5 specifically inhibited leukocyte adhesion, but not rolling, in the brain vasculature.
Conclusions:
- CCL2 and CCL5 play a critical role in EAE by promoting leukocyte adhesion to the brain microvasculature.
- Targeting CCL2 and CCL5-mediated adhesion may be a viable therapeutic strategy for MS.
- These findings clarify the mechanism by which specific chemokines contribute to neuroinflammation in EAE.
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