Clostridium butyricum ameliorates atherosclerotic inflammation through regulation of gut microbiota.

BACKGROUND

Atherosclerosis (AS) is closely associated with gut microbiota that plays an important role in regulating intestinal mucosal barrier function, chronic inflammation, and immune homeostasis. Thus, targeting the modulation of gut microbitoa repesents a promising strategy for the control of AS. Clostridium butyricum (C. butyricum) serving as a kind of probiotics has shown a variety of biological benefits, but it's impact on atherosclerosis remains poorly understood.

METHODS

Sixty male ApoE-/- mice were randomly divided into 4 groups: control group (CON), model group (MOD), C. butyricum control group (CON/CB), and C. butyricum intervention model group (MOD/CB). After 10 weeks of intervention, mice were euthanized and associated indications were investigated.

RESULTS

C. butyricum ameliorated dyslipidemia and attenuated atherosclerotic plaque formation in ApoE-/- mice. This intervention reshaped the gut microbial community and enhanced intestinal barrier integrity. These changes were accompanied by decreased levels of pro-inflammatory cytokines IL-6 and TNF-α, increased anti-inflammatory cytokine IL-10, suppression of Th1/Th17 responses, promotion of Th2/Treg populations, and polarization of macrophages toward the M2 phenotype, while monocyte subsets remained unchanged. Mechanistically, C. butyricum inhibited the LPS/TLR4/NF-κB signaling pathway. Correlation analysis revealed significant associations among gut microbial composition, lipid profiles and inflammation.

CONCLUSION

C. butyricum intervention may exert anti-AS effects by reshaping gut homeostasis via the regulation of immune cells, providing a potential strategy for clinical treatment.