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Altered hepatic clearance and killing of Candida albicans in the isolated perfused mouse liver model
R T Sawyer1, M N Horst, R E Garner
1Mercer University School of Medicine, Macon, Georgia 31207.
Abstract:
The adherence of Candida albicans was studied in situ by using the perfused mouse liver model. After exhaustive washing, 10(6) C. albicans were infused into mouse livers. At the time of recovery, 62 +/- 5% (mean +/- standard error of the mean) of the infused C. albicans were recovered from the liver and 14 +/- 3% were recovered from the effluent for a total recovery of 76 +/- 4%. This indicates that 86 +/- 3% of the original inoculum was trapped by the liver and that 24 +/- 4% was killed within the liver. Chemical pretreatment of C. albicans with 8 M urea, 12 mM dithiothreitol, 2% beta-mercaptoethanol, 1% sodium dodecyl sulfate, 10% Triton X-100, or 3 M potassium chloride or enzyme pretreatment with alpha-mannosidase, alpha-chymotrypsin, subtilisin, beta-N-acetyl-glucosaminidase, pronase, trypsin, papain, or lipase did not alter adherence of C. albicans to hepatic tissue. By contrast, pepsin pretreatment significantly decreased hepatic trapping. Simultaneous perfusion with either 100 mg of C. albicans glycoprotein per liter or 100 mg of C. albicans mannan per liter also decreased trapping. Furthermore, both substances eluted previously trapped C. albicans from hepatic tissue. Chemical pretreatment with 8 M urea, 12 mM dithiothreitol, or 3 M KCI or enzymatic pretreatment with alpha-mannosidase, subtilisin, alpha-chymotrypsin, or papain increased killing of C. albicans three- to fivefold within hepatic tissue. The data suggest that mannose-containing structures on the surface of C. albicans, for example. mannans or glucomannoproteins, mediate adherence of C. albicans within the liver. Indirectly, chemical and enzymatic pretreatment renders C. albicans more susceptible to hepatic killing.
Insights
Candida albicans adherence to the liver is mediated by mannose-containing surface structures. Pretreatment affecting these structures increased fungal killing within the liver.
Area of Science:
- Mycology
- Immunology
- Hepatology
Background:
- Candida albicans is an opportunistic fungal pathogen.
- Understanding fungal adherence to host tissues is crucial for developing anti-adherence strategies.
Purpose of the Study:
- To investigate the mechanisms of Candida albicans adherence to hepatic tissue in situ.
- To identify specific fungal surface components involved in liver trapping.
Main Methods:
- Utilized a perfused mouse liver model to study Candida albicans adherence.
- Administered various chemical and enzymatic pretreatments to C. albicans before liver perfusion.
- Quantified fungal recovery from liver tissue and effluent, and assessed fungal killing.
Main Results:
- The liver trapped 86% of infused Candida albicans, with 24% killed.
- Pepsin pretreatment, C. albicans glycoprotein, and mannan significantly reduced liver trapping.
- Chemical and enzymatic pretreatments increased C. albicans killing by 3-5 fold.
Conclusions:
- Mannose-containing surface structures (mannans, glucomannoproteins) mediate Candida albicans adherence to the liver.
- Disruption of these structures enhances fungal susceptibility to hepatic killing mechanisms.
