The Journal of Experimental Medicine
Aegean Conferences: 2009 Conferences
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Published online 31 May 2005 doi:10.1084/jem.20050054
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 11, 1761-1769
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ARTICLE

 Recruitment of Gr-1+ monocytes is essential for control of acute toxoplasmosis

Paul M. Robben1, Marie LaRegina2, William A. Kuziel3, and L. David Sibley1

1 Department of Molecular Microbiology, Center for Infectious Diseases
2 Division of Comparative Medicine, Washington University School of Medicine, St. Louis, MO 63110
3 Section of Molecular Genetics and Microbiology, The University of Texas at Austin, Austin, TX 78712

CORRESPONDENCE L. David Sibley: sibley{at}borcim.wustl.edu

Circulating murine monocytes comprise two largely exclusive subpopulations that are responsible for seeding normal tissues (Gr-1–/CCR2–/CX3CR1high) or responding to sites of inflammation (Gr-1+/CCR2+/CX3CR1lo). Gr-1+ monocytes are recruited to the site of infection during the early stages of immune response to the intracellular pathogen Toxoplasma gondii. A murine model of toxoplasmosis was thus used to examine the importance of Gr-1+ monocytes in the control of disseminated parasitic infection in vivo. The recruitment of Gr-1+ monocytes was intimately associated with the ability to suppress early parasite replication at the site of inoculation. Infection of CCR2–/– and MCP-1–/– mice with typically nonlethal, low doses of T. gondii resulted in the abrogated recruitment of Gr-1+ monocytes. The failure to recruit Gr-1+ monocytes resulted in greatly enhanced mortality despite the induction of normal Th1 cell responses leading to high levels of IL-12, TNF-{alpha}, and IFN-{gamma}. The profound susceptibility of CCR2–/– mice establishes Gr-1+ monocytes as necessary effector cells in the resistance to acute toxoplasmosis and suggests that the CCR2-dependent recruitment of Gr-1+ monocytes may be an important general mechanism for resistance to intracellular pathogens.

Abbreviations used: BMM, BM-derived macrophages; CNS, central nervous system; Tip-DC, TNF/inducible nitric oxide synthase–producing DC.

W.A. Kuziel's present address is Autoimmunne and Inflammatory Diseases, Protein Design Laboratories, Inc., Fremont, CA 94555.


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