Effect of N-acetylglucosamine on function of peritoneal leukocytes.
OBJECTIVE
To compare effects of N-acetylglucosamine (NAG)-based and glucose-based dialysis fluids on the function of peritoneal leukocytes in conditions of peritoneal dialysis.


METHODS
In vitro experiments on ex vivo isolated rat peritoneal leukocytes.


METHODS
Peritoneal leukocytes were isolated from rats on chronic peritoneal dialysis. On alternate days, fluid exchanges were performed with NAG-based or glucose-based dialysis solutions. After a 4-hour dwell, dialysate was drained and peritoneal leukocytes were incubated in vitro +/- lipopolysaccharide (LPS). Production of nitrites (index of NO synthesis), tumor necrosis factor alpha (TNFalpha), interleukin-1beta (IL-1beta), and interferon gamma (IFN-gamma) by unstimulated or stimulated peritoneal leukocytes originating from NAG-based or glucose-based fluid was measured.


RESULTS
Dialysate cell count was lower during exchanges with NAG-based fluid (2113+/-615 cells/microL) as compared to glucose-based fluid (3643+/-1108 cells/microL; p < 0.01). Differential cell count was similar in both studied groups. Unstimulated peritoneal leukocytes from NAG-based dialysate produced more NO (nitrites) (0.65+/-0.07 micromol per 10(6) cells) than did cells from glucose-based dialysate (0.26+/-0.09 micromol per 106 cells, p < 0.01). Stimulated peritoneal leukocytes from NAG-based dialysate produced more cytokines than did cells from glucose-based dialysate: TNFalpha, 135.2+/-37.0 pg versus 70.2+/-21.8 pg per 10(6) cells respectively, p < 0.01; IL-1beta, 143.2+/-60.9 pg versus 99.1+/-22.4 pg per 10(6) cells respectively, p < 0.05; IFN-gamma, 16.2+/-12.5 pg versus 6.0+/-1.8 pg per 10(6) cells respectively, p < 0.01.


CONCLUSIONS
We demonstrated that rat peritoneal leukocytes exposed in vivo to NAG-based dialysis fluid have better ability to produce inflammatory mediators than do peritoneal leukocytes from the same donor, but exposed in vivo to glucose-based dialysis solution.
Kuzlan-Pawlaczyk
M
M
Department of Pathophysiology, Poznan Medical School, Poland.
Pawlaczyk
K
K
Wieczorowska-Tobis
K
K
Polubinska
A
A
Wisniewska
J
J
Wu
G
G
Tam
P
P
Breborowicz
A
A
D000117:Acetylglucosamine / Q000494:pharmacology*; D000818:Animals; D002452:Cell Count; D002478:Cells, Cultured; D015314:Dialysis Solutions / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D007371:Interferon-gamma / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010529:Peritoneal Cavity / Q000166:cytology*; D010530:Peritoneal Dialysis; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D015314:Dialysis Solutions; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D005947:Glucose; D000117:Acetylglucosamine