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Clinical and Diagnostic Laboratory Immunology, 03 1994, 227-231, Vol 1, No. 2
Copyright © 1994 by the American Society for Microbiology. All rights reserved.

Primary and secondary granule release by polymorphonuclear leukocytes exposed to peritoneal dialysis effluent

I Daniels, SP Crouch, MA Lindsay, AG Morgan, RP Burden and J Fletcher
Medical Research Centre, City Hospital, Nottingham, United Kingdom.

Peritoneal dialysis effluent from patients with end-stage renal failure contains a low-molecular-weight solute that inhibits the killing of phagocytosed Staphylococcus epidermidis by polymorphonuclear leukocytes (PMN). This observation has been investigated by using luciginen- enhanced chemiluminescence to measure PMN NADPH oxidase activity, CD11b/CD18 expression and lactoferrin release to measure secondary granule discharge, and cellular levels of beta-glucuronidase (EC 3.2.1.31) to measure changes in primary granules. Peritoneal dialysis effluent had no effect on the loss of intracellular beta-glucuronidase from normal unstimulated PMN or from PMN stimulated with S. epidermidis. It did, however, cause a concentration-dependent (0 to 70%; vol/vol) increase in expression of CD11b/CD18 and NADPH oxidase activity. CD11b/CD18 expression increased over 20 min before starting to plateau. Release of lactoferrin by the same cells demonstrated a strong positive correlation with integrin expression (P < 0.001, Spearman's rank correlation coefficient). When dialysis effluent- treated PMN were stimulated with formyl-methionylleucylphenylalanine, integrin expression, release of lactoferrin, and NADPH oxidase activity were greater than in PMN treated with formyl- methionylleucylphenylalanine alone. Under these conditions, a concentration-dependent increase in CD11b/ CD18 and lactoferrin release were observed only at a concentration between 0 and 30% (vol/vol) dialysis effluent, while a concentration-dependent increase in oxidase activity was seen at a concentration between 0 and 70% (vol/vol). The results suggest that dialysis effluent does not affect PMN primary granule release but does cause increased release of secondary granules and an increase in NADPH oxidase activity in both unstimulated and stimulated PMN.

This article has been cited by other articles:

• Daniels, I., Fletcher, J., Haynes, A. P. (1999). Role of p38 in the Priming of Human Neutrophils by Peritoneal Dialysis Effluent. CVI 6: 878-884 [Abstract] [Full Text]  
• Daniels, I., Lindsay, M. A., Keany, C. I. C., Burden, R. P., Fletcher, J., Haynes, A. P. (1998). Role of Arachidonic Acid and Its Metabolites in the Priming of NADPH Oxidase in Human Polymorphonuclear Leukocytes by Peritoneal Dialysis Effluent. CVI 5: 683-689 [Abstract] [Full Text]