ArticleJournal of clinical biochemistry and nutrition2026
Mechanism of enteral nutrition in regulating Tfh/Tfr immune imbalance in colorectal cancer via the TLR4 signaling pathway.
Article in Journal of clinical biochemistry and nutrition, 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
This study aims to investigate the regulatory effects and underlying mechanisms of enteral nutrition (EN) on colorectal cancer (CRC). An inflammatory colorectal tumor model was established in mice using the azoxymethane-dextran sulfate sodium method. The mice were divided into groups including a model group and groups treated with EN or EN plus the Toll-like receptor 4 (TLR4) activator lipopolysaccharide. The T follicular helper/T follicular regulatory (Tfh/Tfr) cell ratios in splenic tissues were analyzed by flow cytometry. Protein expression related to the TLR4 pathway and cytokines in colonic tissues was assessed by Western blotting and quantitative real-time polymerase chain reaction. Histopathological changes were evaluated using hematoxylin-eosin staining. The proportion of Tfh cells to Tfr cells is significantly imbalanced in CRC, and this imbalance was corrected following EN treatment. This correction of Tfh/Tfr imbalance was found to inhibit tumor growth, suggesting that the regulatory effect of EN on CRC may be mediated through the modulation of the Tfh/Tfr cell balance. At the molecular level, we discovered that EN was found to suppress the activation of the TLR4 signaling pathway. Furthermore, the addition of lipopolysaccharide abolished the effects of EN, indicating that the regulation of the Tfh/Tfr cell ratio by EN is mediated through the TLR4 signaling pathway. This study provides evidence that EN can inhibit the progression of CRC, potentially by regulating Tfh/Tfr immune imbalance via the TLR4 signaling pathway. These findings highlight the potential of EN as a therapeutic strategy for CRC treatment.
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