This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ellerbroek, P. M. Articles by Coenjaerts, F. E. J. Search for Related Content PubMed PubMed Citation Articles by Ellerbroek, P. M. Articles by Coenjaerts, F. E. J.

 Previous Article  |  Next Article 

Infection and Immunity, September 2002, p. 4762-4771, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.4762-4771.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Cryptococcal Glucuronoxylomannan Inhibits Adhesion of Neutrophils to Stimulated Endothelium In Vitro by Affecting Both Neutrophils and Endothelial Cells

Division of Acute Medicine and Infectious Diseases,¹ Eijkman Winkler Institute for Microbiology, University Medical Centre Utrecht, Utrecht,² Department of Experimental Immunohematology, Central Laboratory of Blood Transfusion, Sanquin Blood Supply Foundation, and Department of Hematology, Academical Medical Center, Amsterdam, The Netherlands³

Received 11 February 2002/ Returned for modification 10 April 2002/ Accepted 4 June 2002

Cryptococcal infections are often characterized by a paucity of leukocytes in the infected tissues. Previous research has shown that the capsular polysaccharide glucuronoxylomannan (GXM) inhibits leukocyte migration. In this study we investigated whether the capsular polysaccharide GXM affects the migration of neutrophils (polymorphonuclear leukocytes [PMN]) through the endothelium by interfering with adhesion in a static adhesion model. Pretreatment of PMN with GXM inhibited PMN adhesion to tumor necrosis factor alpha (TNF-)-stimulated endothelium up to 44%. Treatment of TNF--stimulated endothelium with GXM led to a 27% decrease in PMN adhesion. GXM treatment of both PMN and endothelium did not have an additive inhibitory effect. We demonstrated that GXM-induced L-selectin shedding does not play an important role in the detected inhibition of adhesion. L-selectin was still present on PMN in sufficient amounts after GXM treatment, since it could be further inhibited by blocking antibodies. Furthermore, blocking of GXM-related L-selectin shedding did not abolish the GXM-related inhibition of adhesion. GXM most likely exerts its effect on PMN by interfering with E-selectin-mediated binding. The use of blocking monoclonal antibodies against E-selectin, which was shown to decrease adhesion in the absence of GXM, did not cause additive inhibition of PMN adhesion after GXM pretreatment. The use of blocking antibodies also demonstrated that the inhibiting effect found after GXM treatment of endothelium probably involves interference with both intercellular adhesion molecule-1 and E-selectin binding.

Editor: B. B. Finlay

This article has been cited by other articles:

• Ellerbroek, P. M., Lefeber, D. J., van Veghel, R., Scharringa, J., Brouwer, E., Gerwig, G. J., Janbon, G., Hoepelman, A. I. M., Coenjaerts, F. E. J. (2004). O-Acetylation of Cryptococcal Capsular Glucuronoxylomannan Is Essential for Interference with Neutrophil Migration. J. Immunol. 173: 7513-7520 [Abstract] [Full Text]  
• Haggar, A., Ehrnfelt, C., Holgersson, J., Flock, J.-I. (2004). The Extracellular Adherence Protein from Staphylococcus aureus Inhibits Neutrophil Binding to Endothelial Cells. Infect. Immun. 72: 6164-6167 [Abstract] [Full Text]