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Infection and Immunity, November 1999, p. 5626-5633, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Endothelial Adhesion Molecule Expression and Its Inhibition by Recombinant Bactericidal/Permeability-Increasing Protein Are Influenced by the Capsulation and Lipooligosaccharide Structure of Neisseria meningitidis

Garth L. J. Dixon,1,* Robert S. Heyderman,2 Karolena Kotovicz,1 Dominic L. Jack,1 Svein R. Andersen,3 Ulrich Vogel,4 Matthias Frosch,4 and Nigel Klein1

Immunobiology Unit, Institute of Child Health, London,1 Department of Pathology and Microbiology, School of Medical Sciences, Bristol,2 and The Edward Jenner Institute for Vaccine Research Compton, Newbury,3 United Kingdom, and Institut für Hygiene und Mikrobiologie, Universität Würzburg, 97080 Würzburg, Germany4

Received 19 May 1999/Returned for modification 1 July 1999/Accepted 12 August 1999

Vascular endothelial injury is responsible for many of the clinical manifestations of severe meningococcal disease. Binding and migration of activated host inflammatory cells is a central process in vascular damage. The expression and function of adhesion molecules regulate interactions between leukocytes and endothelial cells. Little is known about how meningococci directly influence these receptors. In this study we have explored the effect of Neisseria meningitidis on endothelial adhesion molecule expression and found this organism to be a potent inducer of the adhesion molecules CD62E, ICAM-1, and VCAM-1. Exposure of endothelium to a serogroup B strain of Neisseria meningitidis, B1940, and a range of isogenic mutants revealed that lipooligosaccharide (LOS) structure and capsulation influence the expression of adhesion molecules. Following only a brief exposure (15 min) to the bacteria, there were large differences in the capacity of the different mutants to induce vascular cell adhesion molecules, with the unencapsulated and truncated LOS strains being most potent (P < 0.05). Furthermore, the pattern of cell adhesion molecule expression was different with purified endotoxin from that with intact bacteria. Meningococci were more potent stimuli of CD62E expression than was endotoxin, whereas endotoxin was at least as effective as meningococci in inducing ICAM-1 and VCAM-1. The effect of bactericidal/permeability increasing protein (rBPI21), an antibacterial molecule with antiendotoxin properties, was also dependent on LOS structure. The strains which possessed a truncated or nonsialylated LOS, whether capsulated or not, were more sensitive to the inhibitory effects of rBPI21. These findings could have important implications for the use of antiendotoxin therapy in meningococcal disease.

* Corresponding author. Mailing address: Immunobiology Unit, Institute of Child Health, London WC1N 1EH, United Kingdom. Phone: 44-171-905-2307. Fax: 44-171-813-8494. E-mail: G.dixon{at}ich.ucl.ac.uk.

Infection and Immunity, November 1999, p. 5626-5633, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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