INTRODUCTION: Sepsis is a life-threatening condition that often leads to organ dysfunction and systemic inflammation, with gut microbiota dysbiosis playing a crucial role in its pathogenesis. The role of (), a potentially pathogenic bacterium, in sepsis remains unclear. METHODS: We first assessed the abundance of in the feces of septic mice and patients using qPCR. Mice were then orally gavaged with (2 × 10 CFU/mouse/day) for 7 consecutive days followed by cecal ligation and puncture (CLP) surgery. We monitored survival, assessed organ damage, and measured inflammation. Peritoneal macrophages were isolated to analyze the phosphorylation of key MAPK and NF-κB signaling pathways. Finally, oxidative stress levels in the liver, lungs, and kidneys were evaluated, measuring markers such as GSH, CAT, and SOD. RESULTS: The abundance of was significantly increased in the feces of both septic mice and patients. Supplementation with exacerbated sepsis in mice, resulting in lower survival rates, more severe organ damage, and heightened inflammation. Phosphorylation of MAPK and NF-κB pathways in peritoneal macrophages was significantly enhanced. Additionally, amplified oxidative stress across multiple organs, as indicated by increased ROS levels and decreased antioxidant enzyme activity. CONCLUSION: Our findings suggest that exacerbates the progression of sepsis by enhancing inflammation, activating key immune signaling pathways, and increasing oxidative stress. These processes contribute to organ dysfunction and increased mortality, highlighting the potential pathogenic role of in sepsis.