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Obesity induces gut leakage and elevates serum lipopolysaccharide (LPS), a major cell wall component of Gram-negative bacteria, through gut translocation. Because  Candida albicans  is prominent in human gut but not in mouse,  C. albicans , a source of (1→3)-β- D -glucan (BG) in gut contents, was administered in high-fat diet (HFD)–induced obese mice at 1 week before sepsis induction by cecal ligation and puncture (CLP). As such, sepsis in  Candida -administered obese mice was more severe than obese mice without  Candida  as determined by mortality, organ injury (liver and kidney), serum cytokines, gut leakage, endotoxemia, serum BG, and fecal Gram-negative bacteria (microbiome analysis). Mice subjected to CLP and fed a HFD, but not treated with  Candida  demonstrated a similar mortality to non-obese mice with more severe gut leakage and higher serum cytokines.  In vitro  experiments demonstrated that LPS plus BG (LPS + BG) induced higher supernatant cytokines from hepatocytes (HepG2) and macrophages (RAW264.7), compared with the activation by each molecule alone, and were amplified by palmitic acid, a representative saturated fatty acid. The energy production capacity of HepG2 cells was also decreased by LPS + BG compared with LPS alone as evaluated by extracellular flux analysis. However,  Lactobacillus rhamnosus  L34 (L34) improved sepsis, regardless of  Candida  administration, through the attenuation of gut leakage and gut dysbiosis. In conclusion, an impact of gut  Candida  was demonstrated by  Candida  pretreatment in obese mice that worsened sepsis through (1) gut dysbiosis–induced gut leakage and (2) amplified systemic inflammation due to LPS, BG, and saturated fatty acid.

frontiers in immunology

Candida Administration Worsens Cecal Ligation and Puncture-Induced Sepsis in Obese Mice Through Gut Dysbiosis Enhanced Systemic Inflammation, Impact of Pathogen-Associated Molecules From Gut Translocation and Saturated Fatty Acid