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This research investigates how gut-derived metabolites influence allergic airway inflammation and the underlying mechanisms.

Gut-derived cinnamic acid limits allergic airway inflammation via the SAT1-spermidine-eIF5A hypusination axis

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This research investigates how gut-derived metabolites influence allergic airway inflammation and the underlying mechanisms.
Oral administration of viable Leuconostoc mesenteroides MY2024 in an animal model.
Measurement of Th2-driven eosinophilic asthma markers following ovalbumin exposure.
Analysis of colonic STAT1-SAT1 signaling and systemic spermidine levels.
Viable MY2024 significantly reduced OVA-induced AAI by attenuating M2-like macrophage activation.
Increased cinnamic acid from MY2024 led to enhanced spermidine catabolism and decreased eIF5A hypusination.
Protective effects were observed even in microbiota-depleted mice, indicating a direct metabolic influence.

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Randomized trial demonstrates that gut-derived cinnamic acid reduces allergic airway inflammation, suggesting a novel therapeutic pathway.

He et al. (2026) studied this question.

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Randomized trial demonstrates that gut-derived cinnamic acid reduces allergic airway inflammation, suggesting a novel therapeutic pathway.