Iron induces B cell pyroptosis through Tom20–Bax–caspase–gasdermin E signaling to promote inflammation post‑spinal cord injury

Journal of Neuroinflammation, 2023 · DOI: https://doi.org/10.1186/s12974-023-02848-0 · Published: July 5, 2023

Simple Explanation

This study investigates the role of B lymphocytes in immune inflammatory responses after spinal cord injury (SCI). It aims to determine the effect of SCI on spleen function and B cell levels. The research explores the mechanism of immunosuppression after SCI, focusing on iron ions and their impact on B cell pyroptosis. The study uses in vivo and in vitro experiments to clarify these relationships. The ultimate goal is to identify a novel immune inflammatory response mechanism induced by SCI, potentially providing a new key target for SCI treatment.

Study Duration

Not specified

Participants

Female C57BL/6 mice (6–8 weeks)

Evidence Level

Not specified

Key Findings

1
Spinal cord injury (SCI) can damage spleen function and lead to a decrease in B cell levels.
2
SCI upregulates the expression of Tom20 protein in the mitochondria of B cells.
3
Iron overload activates the Tom20–Bax–caspase–GSDME pathway after SCI, inducing B cell pyroptosis and promoting inflammation.

Research Summary

This study investigates the role of iron-induced B cell pyroptosis in promoting inflammation after spinal cord injury (SCI). The researchers found that SCI damages spleen function, leading to a decrease in B cell levels and an upregulation of Tom20 protein expression in B cell mitochondria. They discovered that SCI regulates iron ion concentration, activating the Tom20–Bax–caspase–GSDME pathway to induce B cell pyroptosis. Iron ions aggravated B cell pyroptosis by activating this pathway. The study concludes that iron overload activates the Tom20–Bax–caspase–GSDME pathway after SCI, inducing B cell pyroptosis, promoting inflammation, and aggravating SCI-related changes. This suggests a novel mechanism for immune inflammatory response induction after SCI.

Practical Implications

Therapeutic Target

The Tom20–Bax–caspase–GSDME pathway may represent a new key target for the treatment of SCI.

Pharmacological Intervention

Deferoxamine (DFO) can reduce inflammation and promote repair after SCI by inhibiting Tom20–Bax–caspase–GSDME-induced B cell pyroptosis.

Clinical Relevance

Understanding the role of iron and B cell pyroptosis may lead to improved strategies for managing inflammation and promoting recovery in SCI patients.

Study Limitations

1
The precise details of how DFO promotes repair after SCI remain unclear.
2
The relationship between the GSDMD pathway and iron-induced B pyroptosis warrants further exploration.
3
The mechanisms by which ID may promote the metabolic excretion of iron ions or other forms of transfer in mice with SCI require further investigation.

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