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Neutrophil Resolvin E1 Receptor Expression and Function in Type 2 Diabetes
Marcelo O Freire1,2, Jesmond Dalli3, Charles N Serhan3
1Department of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA 02142.
Journal of Immunology (Baltimore, Md. : 1950)
|December 21, 2016
Summary
Resolving inflammation in type 2 diabetes involves specialized lipid mediators like resolvin E1 (RvE1). RvE1 restores neutrophil function and promotes resolution signals, offering therapeutic potential for metabolic dysregulation.
Area of Science:
- Immunology
- Metabolic Diseases
- Lipid Mediators
Background:
- Unresolved inflammation links metabolic dysregulation and immune dysfunction in type 2 diabetes.
- Specialized proresolving lipid mediators, such as resolvin E1 (RvE1), are crucial for acute inflammation resolution.
- RvE1 interacts with G protein-coupled receptors BLT-1 and ERV-1/ChemR23 on immune cells.
Purpose of the Study:
- To investigate novel actions of RvE1 and neutrophil receptor expression patterns in type 2 diabetes.
- To elucidate the role of RvE1 in regulating neutrophil function and inflammation resolution in the context of type 2 diabetes.
Main Methods:
- Analysis of neutrophil receptor expression (BLT-1, ERV-1) in healthy subjects and type 2 diabetes patients.
- Stimulation assays using TNF-α and LPS to assess ERV-1 expression and RvE1's counteracting effects.
- Measurement of ribosomal S6 phosphorylation to determine functional ERV-1 activity.
- Receptor-antagonism experiments to identify mediating receptors for signaling pathways.
- Metabololipidomics to characterize serum inflammatory profiles.
- Assessment of cell phagocytosis and dose-response studies for RvE1 activation of resolution signals.
Main Results:
- Neutrophils from type 2 diabetes patients exhibit altered BLT-1 and ERV-1 expression compared to healthy controls.
- RvE1 counteracted pro-inflammatory cytokine-induced ERV-1 overexpression and activated phagocytosis and resolution signals.
- RvE1-mediated ribosomal S6 phosphorylation was dependent on BLT-1 in healthy neutrophils and ERV-1 in diabetic neutrophils.
- Diabetic serum displayed a pro-inflammatory metabololipidomic profile.
- Phagocytosis was impaired in type 2 diabetes and required RvE1 for activation; higher RvE1 doses were needed for resolution signaling in diabetic neutrophils.
Conclusions:
- RvE1 plays a critical role in resolving inflammation and restoring neutrophil function in type 2 diabetes.
- RvE1 effectively rescues dysregulated neutrophil receptor profiles and promotes resolution signals.
- These findings highlight the therapeutic potential of RvE1 in managing inflammation associated with type 2 diabetes.
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