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β-Glucan Activates Microglia without Inducing Cytokine Production in Dectin-1-Dependent Manner

Vaibhav B. Shah^*, Yongcheng Huang^*, Rohan Keshwara^*, Tammy Ozment-Skelton, David L. Williams and Lakhu Keshvara^1,*

^* Division of Pharmacology, College of Pharmacy, Ohio State University, Columbus, OH 43210; and Department of Surgery, College of Medicine, East Tennessee State University, Johnson City, TN 37614

Microglia are the resident mononuclear phagocytic cells that are critical for innate and adaptive responses within the CNS. Like other immune cells, microglia recognize and are activated by various pathogen-associated molecular patterns. β-glucans are pathogen-associated molecular patterns present within fungal cell walls that are known to trigger protective responses in a number of immune cells. In an effort to better understand microglial responses to β-glucans and the underlying response pathways, we sought to determine whether Dectin-1, a major β-glucan receptor recently identified in leukocytes, plays a similar role in β-glucan-induced activation in microglia. In this study, we report that Dectin-1 is indeed expressed on the surface of murine primary microglia, and engagement of the receptor with particulate β-glucan resulted in an increase in tyrosine phosphorylation of spleen tyrosine kinase, a hallmark feature of the Dectin-1 signaling pathway. Moreover, phagocytosis of β-glucan particles and subsequent intracellular production of reactive oxygen species were also mediated by Dectin-1. However, unlike in macrophages and dendritic cells, β-glucan-mediated microglial activation did not result in significant production of cytokines or chemokines; thus, the interaction of microglial Dectin-1 with glucan elicits a unique response. Our results suggest that the Dectin-1 pathway may play an important role in antifungal immunity in the CNS.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Address correspondence and reprint requests to Dr. Lakhu Keshvara, Division of Pharmacology, College of Pharmacy, 500 West 12th Avenue, Columbus, OH 43210. E-mail address: Keshvara.1{at}osu.edu

² Abbreviations used in this paper: PAMP, pathogen-associated molecular pattern; ROS, reactive oxygen species; SFK, Src family kinase; Syk, spleen tyrosine kinase.

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