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The Aryl Hydrocarbon Receptor Is Required for Optimal Resistance to Listeria monocytogenes Infection in Mice¹

Lewis Zhichang Shi, Nancy G. Faith, Yumi Nakayama, Makulasiddappa Suresh, Howard Steinberg and Charles J. Czuprynski^2,*,

^* Department of Pathobiological Sciences, and Food Research Institute, College of Agriculture and Life Sciences, and the Molecular and Environmental Toxicology Center, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53705

The aryl hydrocarbon receptor (AhR) is part of a powerful signaling system that is triggered by xenobiotic agents such as polychlorinated hydrocarbons and polycyclic aromatic hydrocarbons. Although activation of the AhR by 2,3,7,8-tetrachlorodibenzo-p-dioxin or certain polycyclic aromatic hydrocarbons can lead to immunosuppression, there is also increasing evidence that the AhR regulates certain normal developmental processes. In this study, we asked whether the AhR plays a role in host resistance using murine listeriosis as an experimental system. Our data clearly demonstrate that AhR null C57BL/6J mice (AhR^–/–) are more susceptible to listeriosis than AhR heterozygous (AhR^+/–) littermates when inoculated i.v. with log-phase Listeria monocytogenes. AhR^–/– mice exhibited greater numbers of CFU of L. monocytogenes in the spleen and liver, and greater histopathological changes in the liver than AhR^+/– mice. Serum levels of IL-6, MCP-1, IFN-, and TNF- were comparable between L. monocytogenes-infected AhR^–/– and AhR^+/– mice. Increased levels of IL-12 and IL-10 were observed in L. monocytogenes-infected AhR^–/– mice. No significant difference was found between AhR^+/– and AhR^–/– macrophages ex vivo with regard to their ability to ingest and inhibit intracellular growth of L. monocytogenes. Intracellular cytokine staining of CD4⁺ and CD8⁺ splenocytes for IFN- and TNF- revealed comparable T cell-mediated responses in AhR^–/– and AhR^+/– mice. Previously infected AhR^–/– and AhR^+/– mice both exhibited enhanced resistance to reinfection with L. monocytogenes. These data provide the first evidence that AhR is required for optimal resistance but is not essential for adaptive immune response to L. monocytogenes infection.

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 This work was supported by funds from the National Public Health Sciences (National Institutes of Health Grant R21AI059656), the United States Department of Agriculture National Research Institute (2005-35201-15313), the National Alliance for Food Safety and Security (58-1935-4450), and the Walter and Martha Renk Endowed Laboratory for Food Safety.

² Address correspondence and reprint requests to Dr. Charles J. Czuprynski, Department of Pathobiological Sciences, 2015 Linden Drive, Madison, WI 53706. E-mail address: czuprync{at}svm.vetmed.wisc.edu

³ Abbreviations used in this paper: AhR, aryl hydrocarbon receptor; bHLH-PAS, basic helix-loop-helix Per-Arnt-Sim; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; ARNT, aryl hydrocarbon receptor nuclear transporter; DMBA, 7,12-dimethylbenz[a]anthracene; PAH, polycyclic aromatic hydrocarbon; CBA, cytometric bead assay.

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