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CCR2 Mediates Homeostatic and Inflammatory Release of Gr1^high Monocytes from the Bone Marrow, but Is Dispensable for Bladder Infiltration in Bacterial Urinary Tract Infection¹

Daniel R. Engel^2,*, Juliane Maurer^*, André P. Tittel^*, Christina Weisheit^*, Taner Cavlar^*, Beatrix Schumak^*, Andreas Limmer^*, Nico van Rooijen, Christian Trautwein, Frank Tacke and Christian Kurts^2,*

^* Institute for Molecular Medicine and Experimental Immunology (IMMEI), Rheinische Friedrich-Wilhelms-Universität, Bonn, Germany; Department of Molecular Cell Biology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands; and Medical Clinic III, University Hospital, Rheinisch-Westfälische Technische Hochschule, Aachen, Germany

CCR2 is thought to recruit monocytes to sites of infection. Two subpopulations of murine blood monocytes differing in Gr1 and CCR2 expression have been described. The exact role of CCR2 in migration of CCR2^lowGr1^low and CCR2^highGr1^high monocytes into nonlymphoid tissue is controversial. In this study, we have addressed this question in a murine model of bacterial urinary tract infection. Only Gr1^high monocytes were recruited into the infected bladder. CCR2 deficiency reduced their frequency in this organ, indicating a requirement of this chemokine receptor. Importantly, CCR2-deficient mice also showed reduced Gr1^high monocyte numbers in the blood, but not in the bone marrow (BM), indicating that CCR2 acted at the step of monocyte release into the circulation. The same was found also in noninfected mice, indicating a further involvement of CCR2 in steady-state BM egress. An additional requirement of CCR2 in monocyte recruitment from the blood into the bladder was excluded by tracking particle-labeled endogenous monocytes and by adoptive transfer of BM-derived monocyte subsets. These findings demonstrate that CCR2 governs homeostatic and infection-triggered release of Gr1^high monocytes from the BM into the blood but is dispensable for recruitment into a nonlymphoid tissue.

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 the Deutsche Forschungsgemeinschaft (Grants Ku1063/4, Ku1063/5, Ku1063/6, and Ta434/2-1).

² Address correspondence and reprint requests to Dr. Daniel R. Engel or Dr. Christian Kurts, Institute of Molecular Medicine and Experimental Immunology, Friedrich-Wilhelms-Universität, 53105 Bonn, Germany. E-mail addresses: daniel.engel{at}uni-bonn.de and ckurts{at}web.de

³ Abbreviations used in this paper: BM, bone marrow; UPEC, uropathogenic Escherichia coli; UTI, urinary tract infection; PMN, polymorphonuclear neutrophilic granulocyte; DC, dendritic cell; clo-lip, clodronate-loaded liposome; Lx, latex.

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