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Infection and Immunity, December 1998, p. 5842-5847, Vol. 66, No. 12
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Modulation of Lipopolysaccharide-Induced Monocyte Activation by Heparin-Binding Protein and Fucoidan

Michael Heinzelmann,1,2,* Hiram C. Polk Jr.,2 and Frederick N. Miller1

Department of Physiology and Biophysics,1 and The Price Institute of Surgical Research, Department of Surgery,2 University of Louisville, School of Medicine, Louisville, Kentucky

Received 15 May 1998/Returned for modification 26 June 1998/Accepted 28 September 1998

Activated polymorphonuclear leukocytes release heparin-binding protein (HBP; also known as CAP37 or azurocidin) from azurophilic granules. HBP is a strong chemoattractant for monocytes that also prolongs monocyte survival and potentiates endotoxin (lipopolysaccharide [LPS])-induced production of tumor necrosis factor alpha (TNF-alpha ). We investigated the binding of fluorescein isothiocyanate-conjugated HBP to human monocytes in the presence of EDTA and the polysaccharide fucoidan. EDTA, which chelates divalent cations, has been widely used to study the role of divalent cations in receptor-ligand interactions or enzyme activity. Fucoidan has been used to inhibit the binding of various ligands to scavenger receptors or selectins. Scavenger receptors are multiligand receptors that mediate endocytosis of proteases, protease-inhibitor complexes, lipoproteins, and LPS-lipid A. Fucoidan also interferes with leukocyte rolling by binding to L-selectins (expressed on leukocytes) and P-selectins (expressed on platelets and endothelium). We demonstrate that the binding of the neutrophil-derived protein HBP to monocytes is inhibited in the presence of EDTA and fucoidan. In addition, fucoidan and EDTA abrogate the enhancing effect of HBP on LPS-induced TNF-alpha production. These data provide supporting evidence that HBP binds to a receptor expressed on monocytes. This receptor is dependent on divalent cations and is possibly related to the scavenger receptor. Furthermore, we demonstrate that fucoidan, by itself, stimulates TNF-alpha release from isolated monocytes in a CD14-independent fashion. This is an important finding for the interpretation of results from studies that use fucoidan to "block" either scavenger receptors or L- or P-selectins.

* Corresponding author. Mailing address: c/o M. Abby, Editorial Office, Department of Surgery, University of Louisville, Louisville, KY 40292. Phone: (502) 852-5442. Fax: (502) 852-8915. E-mail: mheinzelmann{at}bluewin.ch.

Infection and Immunity, December 1998, p. 5842-5847, Vol. 66, No. 12
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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