Bacillus-produced surfactin attenuates chronic inflammation in atherosclerotic lesions of ApoE−/− mice

• Bacillus-produced surfactin induces Tregs to inhibit chronic inflammation and attenuate atherosclerosis in mice.
• Tregs secrete IL-10 and TGF-β to create an anti-inflammatory milieu in the aorta wall for athero-protection.
• Surfactin has potential as a novel immunomodulator against atherosclerosis.

Bacillus-produced surfactin can inhibit acute inflammation in vitro and in vivo. However, there is no report whether surfactin could inhibit chronic inflammation in the atherosclerotic lesions. Apoliprotein E deficient (ApoE−/−) mice (fed on atherogenic diet) were intragastrically administered with surfactin for 9 doses, then the athero-protective effect of surfactin was determined in vivo. The results showed surfactin could induce anti-inflammatory factors such as IgA, transforming growth factor (TGF)-β and interleukin (IL)-10 in the intestine. Further investigation discovered that surfactin also systemically induced CD4+ CD25+ FoxP3+ Tregs in spleen, which could inhibit T cells to produce pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α and interferon (IFN)-γ. The IgG subclass pattern with high titer of IgG1 (Th2-type) but low titer of IgG2a (Th1-type) was also found in the surfactin-treated mice. As a result, the attenuation of chronic inflammation was observed in the surfactin-treated groups accompanying with less TNF-α but more IL-10 in the atherosclerotic lesions. Moreover, surfactin could reduce serum total cholesterol and cholesterol in low-density lipoprotein, and increase serum cholesterol in high-density lipoprotein in mice. Collectively, surfactin could significantly attenuate atherosclerotic lesions on the aorta by restoration of the delicate balance of Th1/Th2 response in mice.

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