|Authors||Plotkin BJ, Paulson D, Chelich A, Jurak D, Cole J, Kasimos J, Burdick JR, Casteel N|
|Journal||J. Med. Microbiol. Volume: 44 Issue: 4 Pages: 277-83|
|Publish Date||1996 Apr|
There is a causal relationship between obesity-associated diabetes and an increased risk of infection. The ability of obese (fa/fa) Zucker rats, a model for non-insulin-dependent diabetes mellitus (NIDDM), to clear Candida albicans from the circulation and tissues was compared to that of lean (Fa/fa, Fa/Fa) Zucker rat controls as a measure of immune function. The ID50 necessary to establish tissue colonisation in lean Zucker rats was 1.18 log10 times greater than that determined for the obese Zucker rats. Nine days after intravenous (i.v.) injection of a yeast suspension, the organs of obese rats had a 10-fold greater yeast/g organ burden than did lean rats. The kidney was determined to be the primary target organ for colonisation. Germ-tube formation by C. albicans occurred at a rate 1.5 times faster in serum from obese rats than in serum from lean rats. Peritoneal polymorphonuclear leucocytes, resident macrophages and thioglycollate-elicited macrophages from lean Zucker rats displayed a significantly higher ability to kill ingested yeast cells than analogous cell populations from obese Zucker rats.