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Published online before print January 13, 2006

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0305150

Received for publication March 13, 2005.
Revised November 3, 2005.
Accepted for publication November 17, 2005.

Article

The effect of PGG--glucan on neutrophil chemotaxis in vivo

Department of Surgery, Rhode Island Hospital and Brown Medical School, Providence

	Abstract

The -glucans are long-chain polymers of glucose in -(1,3)(1,6) linkages, which comprise the fungal cell wall and stimulate cells of the innate immune system. Previous in vitro studies have shown the ability of -glucan to increase the chemotactic capacity of human neutrophils. The current study examined an in vivo correlate of that observation by testing the hypothesis that systemic -glucan treatment would result in enhanced migration of neutrophils into a site of inflammation and improve antimicrobial function. A model of acute inflammation was used in which polyvinyl alcohol sponges were implanted subcutaneously into the dorsum of rats. Animals treated with -glucan showed a 66 ± 6% and 186 ± 42% increase in wound cell number recovered 6 and 18 h postwounding, respectively. Increased migration did not correlate with increased chemoattractant content of wound fluid, alterations in neutrophil- induced loss of endothelial barrier function, or changes in neutrophil adhesion to endothelial cells. Systemic administration of SB203580 abrogated the enhanced migration by -glucan without altering normal cellular entry into the wound. Studies also showed a priming effect for chemotaxis and respiratory burst in circulating neutrophils isolated from -glucan-treated animals. Heightened neutrophil function took place without cytokine elicitation. Furthermore, -glucan treatment resulted in a 169 ± 28% increase in neutrophil number and a 60 ± 9% decrease in bacterial load in the bronchoalveolar lavage fluid of Escherichia coli pneumonic animals. Taken together, these findings demonstrate that -glucan directly affects the chemotactic capacity of circulating neutrophils through a p38 mitogen-activated protein kinase-dependent mechanism and potentiates antimicrobial host defense.

Key Words: priming • host defense • rat • p38 MAPK

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