Molecular and mechanistic insights into the gut-liver axis in <i>K. pneumoniae</i> infections: current advances and future directions

<i>Klebsiella pneumoniae</i> is an opportunistic Gram-negative pathogen in clinical settings, primarily causing opportunistic infections in hospitals. The prevalence of liver abscess cases caused by hypervirulent <i>K. pneumoniae</i> (hvKP) has significantly increased in recent years, renewing interest in the interaction between this bacterium and the gut-liver axis. Research has shown that <i>K. pneumoniae</i> disrupts intestinal barrier integrity by adhering to and producing virulence factors, leading to bacterial translocation to vital organs such as the liver. This activation of inflammatory signaling pathways triggers systemic infection, exacerbating liver damage and systemic inflammation. The current research still faces key challenges: the molecular mechanism of bacteria crossing the intestinal barrier to reach the liver is not yet clear, the dynamic regulatory network of the gut-liver axis during infection lacks systematic analysis, and insufficient clinical research data limit a comprehensive understanding of its pathogenic mechanism. This review systematically organizes the latest research progress on the interaction between <i>K. pneumoniae</i> infection and the gut-liver axis, with a focus on the breakdown of the intestinal barrier mediated by virulence factors, mechanisms of bacterial translocation, and the collaborative regulatory network of immune cells (such as macrophages and neutrophils) and inflammatory pathways in the gut-liver axis. By analyzing the immune evasion strategies of hvKP and the host-pathogen arms race with host immune responses, it provides theoretical references for a deeper understanding of its pathogenic mechanism and lays the foundation for clinical development of precise intervention strategies targeting inflammatory pathways or intestinal barrier repair.