Pathogenic Potential of Invasive Mucosa‐Associated Klebsiella pneumoniae Isolates in Ulcerative Colitis: Characterization of Virulence Factors and Inflammatory Response

Background Klebsiella pneumoniae has emerged as an opportunistic pathobiont potentially exacerbating ulcerative colitis (UC) through virulence‐mediated inflammation. However, the pathogenic role of invasive mucosa‐associated K. pneumoniae in UC remains underexplored. This study characterizes virulence factors and inflammatory responses in K. pneumoniae isolates from UC patients to elucidate their contribution to disease progression. Methods Mucosa‐associated K. pneumoniae isolates ( n = 62) from UC patients were compared to non‐UC controls. Virulence genes, including kfu , magA , fimH , mrkD , rmpA , ybtS , iutA , iroN , hcp , and vgrG , were investigated via PCR. Adhesion, invasion, and intracellular survival were assessed in Caco‐2 and THP‐1 cells. The relative expression levels of the NOD1 , NOD2 , STAT1 , and NF‐κB genes were assessed using real‐time quantitative PCR. The concentrations of interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and interleukin‐8 (IL‐8) were quantified with enzyme‐linked immunosorbent assay (ELISA) kits. Results UC‐associated K. pneumoniae isolates exhibited higher prevalence of adhesion/invasion genes (e.g., fimH in 77.4% vs. 46.6%) and enhanced adhesive/invasive phenotypes (29% adherent, 16.1% invasive) compared to controls. These strains lacked hypervirulence markers ( rmpA , magA ) but aligned with classical virulent profiles. Invasive isolates upregulated NOD1 , NOD2 , and STAT1 expression and significantly increased IL‐8 secretion ( p < 0.05), amplifying pro‐inflammatory responses. Conclusion Invasive mucosa‐associated K. pneumoniae in UC display distinct virulence traits that promote epithelial invasion and inflammation, potentially driving disease exacerbation. Targeting these pathobionts offers a promising avenue for novel UC therapies.