BackgroundInfantile 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.MethodsA 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.ResultsIESS patients had significantly higher serum HMGB1, TLR4, IL-2, IL-2R, IL-8 and TNF-α than controls (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 ΔPre-Post HMGB1 was a protective factor (P < 0.05).
Frontiers in Immunology published a clinical update in Infectious Disease on 01 May 2026.
The item focuses on Clinical application of HMGB1-TLR4 signaling pathway-mediated neuroinflammatory markers in infantile epileptic spasms syndrome.
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