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Monosodium glutamate induces apoptosis in naive and memory human B cells
Z Jovic1, M Veselinovic, K Vasic
1Institute of Pharmacology and Toxicology, Medical Faculty Nis, University of Nis, Serbia.
Insights
Monosodium glutamate (MSG) induces apoptosis in normal B lymphocytes, affecting both naive and memory cells. This suggests a potential nervous-immune system crosstalk mediated by glutamate receptors, specifically mGluR7, in B cells.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- B lymphocytes play a crucial role in the immune system.
- Glutamate is a primary neurotransmitter in the nervous system.
- Potential interactions between the nervous and immune systems are increasingly recognized.
Purpose of the Study:
- To confirm the presence of metabotropic glutamate receptor 7 (mGluR7) in normal B lymphocytes.
- To investigate the impact of monosodium glutamate (MSG) on B cell apoptosis in vitro.
- To explore the potential role of mGluR7 in mediating MSG-induced B cell apoptosis.
Main Methods:
- B lymphocytes were isolated using magnetic cell sorting with anti-CD19 beads.
- Cells were cultured with varying concentrations of MSG (1-100 mM).
- Apoptosis was assessed via flow cytometry using Annexin V-FITC/Propidium iodide staining.
- Naïve and memory B cell populations were identified using CD27 staining.
- Glutamate receptor (GluR) expression was analyzed by PCR.
Main Results:
- MSG exposure demonstrated a dose-dependent reduction in B cell viability, from 80% at 1 mM to 35% at 100 mM.
- The number of late apoptotic and necrotic B cells increased in a dose-dependent manner with MSG exposure.
- Both CD27- (naïve) and CD27+ (memory) B cell populations were susceptible to MSG-induced apoptosis.
- Basal expression of mGluR7 was detected in unstimulated B cells.
Conclusions:
- Glutamate, likely through mGluR7, induces apoptosis in both naïve and memory B cell populations.
- The study confirms the expression of mGluR7 in B lymphocytes.
- A novel mechanism of nervous-immune system communication involving glutamate as a mediator is proposed.
Abstract:
The aim of this study was to establish the existence of mGluR7 in normal B lymphocytes and analyse the effect of monosodium glutamate (MSG) on B cell apoptosis in vitro. B cells were purified by magnetic cell sorting using anti-CD19-coupled magnetic beads. Cells (10(6)/ml) were cultured with increasing MSG concentrations (1-100 mM). Detection of apoptosis by flow cytometry was performed using the Annexin V-FITC/Propidium iodide (PI) apoptosis detection kit. Naïve and memory B cell population were identified by CD27 staining. Expression of GluRs was determined using PCR. Exposure to increasing MSG concentrations displayed dose dependent effect on B cell viability altogether, ranging from 35% with 100 mM up to 80% with 1 mM MSG. Moreover, the number of late apoptotic cells as well as necrotic cells was dose dependant. Both CD27- as well as CD27+ B cells were affected by MSG. Basal expression of GluRs7 was detected in unstimulated B cells. Glutamate induced apoptosis can be seen in memory as well as naive B cell population and is probably mediated through mGluR7, whose expression in B cells we also confirmed. Our study suggests a new possible mechanism of crosstalk between the nervous and the immune system through glutamate as a potential key mediator (Fig. 4, Ref. 27). Full Text (Free, PDF) www.bmj.sk.
