Clinical application of HMGB1-TLR4 signaling pathway-mediated neuroinflammatory markers in infantile epileptic spasms syndrome

Background Infantile epileptic spasms syndrome (IESS) is a severe age-specific epileptic encephalopathy with unclear pathogenesis, and neuroinflammation is involved in its progression. The HMGB1-TLR4 signaling pathway, a key neuroinflammatory mediator in various epilepsies, has not been studied for its role and clinical biomarker potential in IESS. Methods A retrospective study included 66 IESS patients treated with a modified prednisone regimen and 53 age-matched healthy controls. Serum HMGB1, TLR4, IL-1β, IL-2, IL-2R, IL-8 and TNF-α were detected by ELISA/chemiluminescent immunoassay in IESS patients (pre- and 2-week post-treatment) and controls; clinical data were collected via electronic medical records and follow-up. Results IESS patients had significantly higher serum HMGB1, TLR4, IL-2, IL-2R, IL-8 and TNF-α than controls ( P < 0.05; no IL-1β difference, P >0.05), and these elevated indicators decreased markedly post-treatment ( P < 0.05). Logistic regression showed identified etiology and focal seizures were risk factors for short-term prednisone ineffectiveness, while Δ Pre-Post HMGB1 was a protective factor ( P < 0.05). Long-term follow-up (≥18 months) found identified etiology to be a risk factor for uncontrolled epilepsy and poor neurodevelopment ( P < 0.05); early spasm remission and long-term seizure control were protective factors for neurodevelopment ( P < 0.05). Conclusions The HMGB1-TLR4 pathway mediates neuroinflammation in IESS pathogenesis and may serve as a therapeutic target. A high Δ Pre-Post HMGB1 level was identified as a protective factor against short-term treatment failure of prednisone, indicating that dynamic monitoring of HMGB1 has clinical value for predicting short-term treatment responses to prednisone, though it does not predict long-term seizure control or neurodevelopmental outcomes. Identified etiology is a common risk factor for poor IESS outcomes, highlighting the importance of early etiological screening and sustained seizure control for IESS management.

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Journal
Frontiers in Immunology
Published
2026-05-01
DOI
https://doi.org/10.3389/fimmu.2026.1801505
Primary Topic
Epilepsy research and treatment
Type
article
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article

Clinical application of HMGB1-TLR4 signaling pathway-mediated neuroinflammatory markers in infantile epileptic spasms syndrome

Ruiyan Wang, Zhaoshi Yi, Xingying Zeng, Jianmin Zhong et al.
Frontiers in Immunology
Epilepsy research and treatment
article

Clinical application of HMGB1-TLR4 signaling pathway-mediated neuroinflammatory markers in infantile epileptic spasms syndrome

Ruiyan Wang, Zhaoshi Yi, Xingying Zeng, Jianmin Zhong, Huaping Wu, Hui Chen, Yong Chen
article en

Abstract

Background Infantile epileptic spasms syndrome (IESS) is a severe age-specific epileptic encephalopathy with unclear pathogenesis, and neuroinflammation is involved in its progression. The HMGB1-TLR4 signaling pathway, a key neuroinflammatory mediator in various epilepsies, has not been studied for its role and clinical biomarker potential in IESS. Methods A retrospective study included 66 IESS patients treated with a modified prednisone regimen and 53 age-matched healthy controls. Serum HMGB1, TLR4, IL-1β, IL-2, IL-2R, IL-8 and TNF-α were detected by ELISA/chemiluminescent immunoassay in IESS patients (pre- and 2-week post-treatment) and controls; clinical data were collected via electronic medical records and follow-up. Results IESS patients had significantly higher serum HMGB1, TLR4, IL-2, IL-2R, IL-8 and TNF-α than controls ( P < 0.05; no IL-1β difference, P >0.05), and these elevated indicators decreased markedly post-treatment ( P < 0.05). Logistic regression showed identified etiology and focal seizures were risk factors for short-term prednisone ineffectiveness, while Δ Pre-Post HMGB1 was a protective factor ( P < 0.05). Long-term follow-up (≥18 months) found identified etiology to be a risk factor for uncontrolled epilepsy and poor neurodevelopment ( P < 0.05); early spasm remission and long-term seizure control were protective factors for neurodevelopment ( P < 0.05). Conclusions The HMGB1-TLR4 pathway mediates neuroinflammation in IESS pathogenesis and may serve as a therapeutic target. A high Δ Pre-Post HMGB1 level was identified as a protective factor against short-term treatment failure of prednisone, indicating that dynamic monitoring of HMGB1 has clinical value for predicting short-term treatment responses to prednisone, though it does not predict long-term seizure control or neurodevelopmental outcomes. Identified etiology is a common risk factor for poor IESS outcomes, highlighting the importance of early etiological screening and sustained seizure control for IESS management.

Frontiers in ImmunologyVol. 17
Jiangxi Provincial Children's Hospital (CN)
Good health and well-being
Openalex Percentile: Top 9%
Epilepsy research and treatment
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