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Spermine achieves multi-layered defense against pathogens by regulating immune cell activity, reshaping the immune microenvironment, and enhancing the mucosal barrier.

(1) Activates immune cell function and enhances pathogen clearance efficiency

Spermine can induce macrophages to polarize from the pro-inflammatory M1 type to the anti-inflammatory and pro-repair M2 type, significantly enhancing their phagocytic capacity (phagocytic efficiency increased by 2.7 times in in vitro experiments).

Spermine balances the immune response by promoting Th1 cell differentiation (secreting IFN-γ to enhance cellular immunity) and regulating Treg cell function (maintaining immune tolerance). In a hepatitis B virus (HBV) infection model, spermine increased IFN-γ secretion in CD4⁺ T cells by 2.3-fold, while simultaneously enhancing T cell activity through autophagy and significantly reducing HBV DNA load.

(2) Regulating the inflammatory response to prevent "immune storms"

Suppressing excessive inflammation: Spermine reduces the release of pro-inflammatory factors such as IL-6 and TNF-α by inhibiting the NF-κB pathway. For example, in a lipopolysaccharide (LPS)-stimulated macrophage model, spermine reduced IL-6 levels by 63% while promoting a 45% increase in the secretion of the anti-inflammatory factor IL-10.

Balancing antiviral immunity: In viral infections, spermidine prevents excessive immune activation by regulating the cGAS-STING pathway. Studies have found that spermidine can induce DNA conversion from type B (easily activated cGAS) to type Z (low affinity), reducing the excessive release of type I interferon. In a herpesvirus (HSV-1) infection model, spermidine treatment reduced viral titers by 59% while preventing excessive inflammatory damage to lung tissue.

(3) Strengthen the mucosal barrier and block pathogen invasion

Intestinal mucosal immune regulation: Spermidine maintains intestinal barrier integrity by promoting gut microbiota metabolism (e.g., increasing the abundance of *Lactobacillus rhamnosus*). In a stress-induced irritable bowel syndrome (IBS-D) model, spermidine restores spermidine levels produced by gut microbiota, upregulates the expression of the tight junction protein occludin, reduces intestinal permeability by 52%, and decreases pathogen translocation.

Respiratory mucosal protection: Spermidine clears viral particles by enhancing the autophagy function of respiratory epithelial cells. In an influenza virus infection model, spermidine pretreatment increases the phagocytic rate of viruses by alveolar macrophages by 45%, reduces viral load in the lungs by 61%, and reduces airway obstruction caused by excessive mucus secretion.