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<i>Klebsiella pneumoniae</i> is an opportunistic pathogen and a commensal organism that is possibly enhanced in several conditions with gut dysbiosis, and frequently detectable together with <i>Candida</i> overgrowth. Here, <i>K. pneumoniae</i> with or without <i>Candida albicans</i> was daily orally administered for 3 months in 0.8% dextran sulfate solution-induced mucositis mice and also tested <i>in vitro</i>. As such, <i>Candida</i> worsened <i>Klebsiella-</i>DSS-colitis as demonstrated by mortality, leaky gut (FITC-dextran assay, bacteremia, endotoxemia, and serum beta-glucan), gut dysbiosis (increased Deferribacteres from fecal microbiome analysis), liver pathology (histopathology), liver apoptosis (activated caspase 3), and cytokines (in serum and in the internal organs) when compared with <i>Klebsiella-</i>administered DSS mice. The combination of heat-killed <i>Candida</i> plus <i>Klebsiella</i> mildly facilitated inflammation in enterocytes (Caco-2), hepatocytes (HepG2), and THP-1-derived macrophages as indicated by supernatant cytokines or the gene expression. The addition of heat-killed <i>Candida</i> into <i>Klebsiella</i> preparations upregulated <i>TLR-2</i>, reduced <i>Occludin</i> (an intestinal tight junction molecule), and worsened enterocyte integrity (transepithelial electrical resistance) in Caco-2 and enhanced <i>casp8</i> and <i>casp9</i> (apoptosis genes) in HepG2 when compared with heat-killed <i>Klebsiella</i> alone. In conclusion, <i>Candida</i> enhanced enterocyte inflammation (partly through <i>TLR-2</i> upregulation and gut dysbiosis) that induced gut translocation of endotoxin and beta-glucan causing hyper-inflammatory responses, especially in hepatocytes and macrophages.