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Published on: September 15, 2017
Differential expression of selectins by mouse brain capillary endothelial cells in vitro in response to distinct
Caroline Coisne1, Christelle Faveeuw, Yannick Delplace
1EA 2465-Université d'Artois, Faculté des Sciences Jean Perrin, 62307 Lens, France.
Insights
Selectin expression on the blood-brain barrier (BBB) is controversial. This study found that while resting mouse brain capillary endothelial cells (MBCECs) lack selectins, inflammatory stimuli like LPS and IL-1beta can induce their expression, influencing immune cell entry into the CNS.
Area of Science:
- Neuroimmunology
- Endothelial Cell Biology
- Blood-Brain Barrier Research
Background:
- Lymphocyte trafficking across the blood-brain barrier (BBB) is critical in central nervous system (CNS) inflammatory diseases.
- Adhesion molecules mediate leukocyte entry into the brain, but the role of selectins at the BBB remains unclear.
- Existing research on selectin expression in CNS inflammation presents conflicting findings.
Purpose of the Study:
- To investigate the expression of selectins on mouse brain capillary endothelial cells (MBCECs) in vitro.
- To determine the effects of specific inflammatory stimuli on selectin expression at the BBB.
- To clarify the role of selectins in immune cell infiltration into the CNS.
Main Methods:
- Utilized a syngenic in vitro mouse BBB model using MBCECs.
- Treated MBCECs with lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin-1beta (IL-1β).
- Assessed the expression of E-selectin and P-selectin on MBCECs following inflammatory stimulation.
Main Results:
- MBCECs did not express selectins under basal conditions.
- LPS treatment induced both E-selectin and P-selectin expression on MBCECs.
- IL-1β treatment induced P-selectin but not E-selectin expression, while TNF-α and IFN-γ had no significant effect.
- These findings indicate differential regulation of selectin expression by various inflammatory mediators.
Conclusions:
- Selectin expression at the BBB is not constitutive and is differentially regulated by specific inflammatory cytokines.
- Understanding these differential regulations is crucial for developing targeted therapies for CNS inflammatory and immune-mediated diseases.
- This study contributes to elucidating the molecular mechanisms governing immune cell trafficking across the BBB.
Abstract:
Increased lymphocyte trafficking across blood-brain barrier (BBB) is a prominent and early event in inflammatory and immune-mediated CNS diseases. The adhesion molecules that control the entry of leukocytes into the brain have not been fully elucidated. Although the role of ICAM-1 and VCAM-1 has been well documented, the expression and role of selectins is still a matter of controversy. In a mouse syngenic in vitro BBB model, highly relevant for examining immunological events, mouse brain capillary endothelial cells (MBCECs) do not express selectins. Treatment of MBCECs with LPS, induced E- and P-selectin expression, whereas TNF-alpha or IFN-gamma treatments did not. Finally, P-selectin but not E-selectin expression was induced in IL-1beta treated MBCECs. Thus, our study suggests that diverse inflammatory stimuli could differentially regulate selectin expression at the BBB.
