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T1R1/T1R3 Taste Receptor Suppresses Granulocyte-Mediated Neuroinflammation after Spinal Cord Injury.
- Source :
-
Journal of Neurotrauma . Aug2017, Vol. 34 Issue 15, p2353-2363. 11p. - Publication Year :
- 2017
-
Abstract
- As an active and predominant blood leukocyte population, granulocytes infiltrate into injured spinal cord and produce pro-inflammatory mediators to aggravate neuroinflammation. In the current study, we identify the role of the T1R1/T1R3 receptor in granulocyte-mediated neuroinflammation in a rat spinal cord injury (SCI) model. We found that T1R1 and T1R3 were substantially expressed in both circulating and infiltrating granulocytes. In vitro stimulation of T1R1/T1R3 receptor with L-serine notably reduced production of reactive oxygen species (ROS) and several pro-inflammatory cytokines. To evaluate the role of T1R1/T1R3 receptor in vivo, gurmarin, a selective T1R3 inhibitor, was injected into rats before and after SCI. Gurmarin administration significantly upregulated expression of interleukin (IL)-1β, IL-6, myeloperoxidase, and matrix metallopeptidase 9, as well as production of ROS in infiltrating granulocytes. Signal pathway analysis revealed that gurmarin promoted nuclear factor (NF)-κβ signaling in infiltrating granulocytes. Consistently, cell apoptosis and inflammatory mediator levels at the injury sites were increased by gurmarin, together with higher T lymphocyte recruitment. Our research indicates that the T1R1/T1R3 receptor is an anti-inflammatory receptor for infiltrating granulocytes after SCI. Simulation of T1R1/T1R3 receptor might be a prospective, or at least a supplemental, therapeutic approach to controlling neuroinflammation to promote functional recovery. [ABSTRACT FROM AUTHOR]
- Subjects :
- *LEUCOCYTES
*GRANULOCYTES
*SPINAL cord
*RATS
*CYTOKINES
*MYELOPEROXIDASE
Subjects
Details
- Language :
- English
- ISSN :
- 08977151
- Volume :
- 34
- Issue :
- 15
- Database :
- Academic Search Index
- Journal :
- Journal of Neurotrauma
- Publication Type :
- Academic Journal
- Accession number :
- 124253148
- Full Text :
- https://doi.org/10.1089/neu.2016.4952