Severe trauma, wounds and sepsis result in generalized suppression of host defenses. Mammalian macrophages possess a recently described cell surface receptor that recognizes beta-1,3 polymers of glucose. This beta-glucan receptor provides a means for opsonin- independent recognition and clearance of microorganisms. Binding to beta-glucan receptors potentiates the phagocytic function of macrophages. Receptors for binding the Fc portion of immunoglobulin and the complement receptor are well characterized markers of macrophage activation. These opsonic receptors are known to be compromised in neutrophils from septic animals. The role of the beta-glucan receptor is presently unknown and is the focus of this application. These studies will detail the structure and binding characteristics of the receptor using standard methods to quantitate number and affinity. The expression of beta- glucan will be determined in resting and activated cells from various anatomic sites. Experiments will compare the beta- glucan receptor expression with the expression of opsonic receptors and correlate similarities and differences with activation state and immune function. These studies will test the hypothesis that the non-opsonic beta-glucan receptor plays a greater role in host defense under conditions of compromised opsonin-dependent phagocytosis.

National Institute of Health (NIH)
National Institute of General Medical Sciences (NIGMS)
Research Project (R01)
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Surgery, Anesthesiology and Trauma Study Section (SAT)
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Rhode Island Hospital (Providence, RI)
United States
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Reichner, J S; Fitzpatrick, P A; Wakshull, E et al. (2001) Receptor-mediated phagocytosis of rat macrophages is regulated differentially for opsonized particles and non-opsonized particles containing beta-glucan. Immunology 104:198-206
Harler, M B; Reichner, J (2001) Increased neutrophil motility by beta-glucan in the absence of chemoattractant. Shock 16:419-24
Meszaros, A J; Reichner, J S; Albina, J E (2000) Macrophage-induced neutrophil apoptosis. J Immunol 165:435-41
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Albina, J E; Mastrofrancesco, B; Reichner, J S (1999) Acyl phosphatase activity of NO-inhibited glyceraldehyde-3-phosphate dehydrogenase (GAPDH): a potential mechanism for uncoupling glycolysis from ATP generation in NO-producing cells. Biochem J 341 ( Pt 1):5-9
Harler, M B; Wakshull, E; Filardo, E J et al. (1999) Promotion of neutrophil chemotaxis through differential regulation of beta 1 and beta 2 integrins. J Immunol 162:6792-9
Yauch, R L; Berditchevski, F; Harler, M B et al. (1998) Highly stoichiometric, stable, and specific association of integrin alpha3beta1 with CD151 provides a major link to phosphatidylinositol 4-kinase, and may regulate cell migration. Mol Biol Cell 9:2751-65
Louis, C A; Reichner, J S; Henry Jr, W L et al. (1998) Distinct arginase isoforms expressed in primary and transformed macrophages: regulation by oxygen tension. Am J Physiol 274:R775-82
Reichner, J S; Helgemo, S L; Hart, G W (1998) Recycling cell surface glycoproteins undergo limited oligosaccharide reprocessing in LEC1 mutant Chinese hamster ovary cells. Glycobiology 8:1173-82