ArticleAdvances in radiation oncology2026
Upregulation of S100A8/A9 Potentiates Radiation-Induced Intestinal Injury via MAPK and NF-κB Signaling Pathways.
Article in Advances in radiation oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Radiation-induced intestinal injury (RIII) is a serious complication of radiation therapy without effective therapies. The alarmin, S100A8/A9, a biomarker of gastrointestinal inflammation, is highly elevated following abdominal irradiation (ABI). However, it remains unclear whether it functions as an active driver of RIII pathogenesis. The study aims to assess the effects of S100A8/A9 on the pathogenesis of RIII. Our goal is to identify its dynamic alteration during RIII and determine whether it can be used as a therapeutic target in the injury and repair phases of acute RIII. Methods and Materials: C57BL/6J mice were subjected to ABI, and S100A8/A9 expression was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunofluorescence at multiple time points (days 1, 4, and 8) during RIII. The small-molecule inhibitor, paquinimod, was used to block S100A9 in vivo, and recombinant proteins S100A8/A9 were used in rat intestinal epithelial cell line 6 cells and organoids for in vitro validation. Epithelial regeneration was tracked through lineage tracing assays using Results: S100A8/A9 expression in the mouse intestine was obviously upregulated post-ABI in a time-dependent manner, which started to increase from day 1 and reached the peak on day 4. The increased S100A8/A9 was primarily released from neutrophils infiltrated into the intestinal crypts. Inhibition of S100A8/A9 with paquinimod substantially alleviated irradiation-induced epithelial apoptosis, oxidative stress, and inflammatory responses, although enhancing crypt regeneration and restoration of intestinal barrier integrity. Mechanistically, S100A8/A9 exacerbated irradiation-induced intestinal injury via binding to toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE) receptors and subsequently activating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways. Conclusions: This study identifies S100A8/A9 as a critical pathogenic contributor to acute RIII and provides strong evidence supporting S100A8/A9 as a potential therapeutic target for RIII.
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