肠杆菌科细菌性肝脓肿的病理生理机制： 从肠道定植到全身耗竭

Pathophysiological Mechanisms of Enterobacteriaceae-Associated Pyogenic Liver Abscess: From Intestinal Colonization to Systemic Exhaustion

摘要: 细菌性肝脓肿(PLA)是由细菌引起的严重感染性疾病，其发病率及不良预后风险近年来持续上升，尤以高毒力肺炎克雷伯菌和产ESBLs菌株为主要挑战。研究显示，肠道菌群失调及肠屏障破坏促使细菌经门静脉易位至肝脏，是肝脓肿发生的起始环节；随后肠–肝轴双向紊乱加剧炎症反应并形成恶性循环。感染失控可触发以细胞因子风暴为特征的全身炎症反应综合征，继而导致淋巴细胞减少、免疫功能抑制及营养代谢耗竭，最终进展为脓毒症和多器官功能障碍。本文系统综述了肠杆菌科细菌性肝脓肿从肠道定植到全身免疫营养耗竭的病理生理机制，并探讨了微生物调节、免疫调控及强化营养支持等辅助治疗策略，为优化临床管理和改善预后提供理论依据。

Abstract: Pyogenic liver abscess (PLA) is a severe bacterial infection, whose incidence and risk of poor prognosis have been on the rise in recent years. Hypervirulent Klebsiella pneumoniae and extended-spectrum β-lactamase (ESBLs)-producing strains pose the most prominent challenges in this regard. Studies have demonstrated that intestinal dysbiosis and intestinal barrier disruption facilitate bacterial translocation to the liver via the portal vein, which constitutes the initial step in the development of liver abscess. Subsequent bidirectional dysfunction of the gut-liver axis exacerbates the inflammatory response and forms a vicious cycle. Uncontrolled infection can trigger systemic inflammatory response syndrome (SIRS) characterized by cytokine storm, which in turn leads to lymphopenia, immunosuppression, and metabolic exhaustion. The condition may eventually progress to sepsis and multiple organ dysfunction syndrome (MODS). This review systematically summarizes the pathophysiological mechanisms of Enterobacteriaceae-associated pyogenic liver abscess, ranging from intestinal colonization to systemic immunometabolic exhaustion, and further discusses adjuvant therapeutic strategies such as microbial modulation, immunoregulation, and intensive nutritional support. It is expected to provide a theoretical basis for optimizing clinical management and improving patient prognosis.