BACKGROUND

Candida albicans is a polymorphic fungus that frequently causes systemic infection in postsurgical and trauma patients. Others have reported that Escherichia coli lipopolysaccharide (LPS) acts as a copathogen to enhance the virulence of parenteral C. albicans. Experiments were designed to clarify the effect of parenteral LPS on systemic candidiasis initiated via the oral route.

METHODS

Antibiotic-treated mice were orally inoculated with C. albicans CAF2 (wild-type) or mutant HLC54 (defective in filament formation), and were given 100 microg parenteral LPS 16 h before sacrifice. Separate groups of mice were additionally exposed to intermittent hypoxia prior to LPS. At sacrifice, cecal flora and microbial translocation to the mesenteric lymph nodes were quantified. C. albicans adherence to cultured HT-29 and Caco-2 enterocytes (pretreated with LPS, or calcium-free medium to expose the enterocyte lateral surface, or both) was quantified by enzyme-linked immunoabsorbent assay.

RESULTS

All mice had high numbers of cecal C. albicans, and LPS was associated with an additional increase in cecal concentrations of HLC54 but not CAF2. Translocation of HLC54, but not CAF2, appeared facilitated by hypoxia, but LPS did not facilitate translocation in any treatment group. Exposure of the lateral surface of cultured enterocytes had no effect on C. albicans adherence, although LPS consistently decreased adherence of both C. albicans strains.

CONCLUSIONS

In contrast to experiments where systemic candidiasis was initiated by the parenteral route, parenteral LPS did not act as a copathogen in mice with systemic candidiasis initiated by the oral route, and these results might be related to LPS-induced alterations in C. albicans adherence to host enterocytes.