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International Immunology Advance Access published online on October 4, 2004
International Immunology, doi:10.1093/intimm/dxh169
© 2004 by The Japanese Society for Immunology
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Received July 7, 2004
Accepted August 30, 2004

Article

Constitutive expression of CXCL2/MIP-2 is restricted to a Gr-1high, CD11b+, CD62Lhigh subset of bone marrow derived granulocytes

Sigrid P. Matzer 1, Franz Rödel 2, Robert M. Strieter 3, Martin Röllinghoff 1, and H. Ulrich Beuscher 1*

1 Institute for Clinical Microbiology, Immunology and Hygiene, University of Erlangen, Erlangen, Germany
2 Department of Radiooncology, University of Erlangen, Erlangen, Germany
3 Department of Medicine and Pathology and Laboratory Medicine, UCLA, School of Medicine, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: beuscher{at}mikrobio.med.uni-erlangen.de.


  Abstract

CXCL2/macrophage inflammatory protein (MIP)-2 is an inducible murine chemokine involved in attraction of polymorphonuclear granulocytes to sites of infection. In comparison, its role as constitutive produced chemokine in mice is unclear. The present study aimed to specify the cellular source of constitutively produced CXCL2/MIP-2 and to examine its expression pattern in comparison to other chemokines in peripheral lymphoid tissues as well as bone marrow (BM) of normal mice. The results showed that constitutive expression of CXCL2/MIP-2 mRNA was restricted to BM. As revealed by RT-PCR and FACS analysis, CXCL2/MIP-2 production was restricted to a specialized subset of BM derived Gr-1high granulocytes. This subset was characterized by surface expression of CD11b+, CD62Lhigh and CXCR2+ and accounted for 4-6% of total BM cells. In vitro stimulation of BM cells did not increase the number of CXCL2/MIP-2+ granulocytes. Intracellular CXCL2/MIP-2 was not strictly correlated to surface expression of its receptor, as the majority of the CXCR2+/Gr-1high cells lacked CXCL2/MIP-2 staining. In controls, CXCL1/KC expression was not detected in BM but was found in peripheral tissues in the absence of CXCL2/MIP-2. Together, our results show that CXCL2/MIP-2 and CXCL1/KC are differentially expressed in a tissue specific manner in normal mice and that CXCL2/MIP-2 is produced in a well-defined CD11b+, CD62Lhigh, Gr-1high subset of BM granulocytes, thereby providing a possible explanation for the independent regulation of both chemokines.

Keywords: chemokines; neutrophils; Peyer's patches; spleen.
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