This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jablonska, J.
Right arrow Articles by Weiss, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jablonska, J.
Right arrow Articles by Weiss, S.

 Previous Article  |  Next Article 

Infection and Immunity, January 2007, p. 462-470, Vol. 75, No. 1
0019-9567/07/$08.00+0     doi:10.1128/IAI.00443-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Essential Role of CCL2 in Clustering of Splenic ERTR-9+ Macrophages during Infection of BALB/c Mice by Listeria monocytogenes{triangledown}

Jadwiga Jablonska,1* Kurt E. Dittmar,2 Tanja Kleinke,1 Jan Buer,3,4 and Siegfried Weiss1

Molecular Immunology,1 Molecular Biotechnology,2 Mucosal Immunology, Helmholtz Centre for Infection Research, Inhoffenstraße 7, D-38124 Braunschweig, Germany,3 Institute of Medical Microbiology, Hannover Medical School, Hannover, Germany4

Received 17 March 2006/ Returned for modification 30 June 2006/ Accepted 20 October 2006

Early interactions between pathogens and host cells are often decisive for the subsequent course of infection. Here we investigated early events during infection by Listeria monocytogenes, a ubiquitously occurring facultative intracellular microorganism that exhibits severe pathogenicity, mainly in immunocompromised individuals. We show that the inflammatory chemokine CCL2 is highly up-regulated early after Listeria infection in spleens of BALB/c mice. ERTR-9+ macrophages of the marginal zone were identified as the only infected cells and exclusive producers of CCL2 at the early time point. Consequently, clusters of different cell types were formed around infected ERTR-9+ cells. Metallophilic MOMA-1+ marginal zone macrophages were, however, excluded from the clusters and migrated into the B-cell follicles. Depletion of CCL2 during infection resulted in a different composition of cell clusters in the spleen and increased the mortality rate of treated mice. Interestingly, ERTR-9+ macrophages no longer were part of clusters in such mice but remained at their original location in the marginal zone.

* Corresponding author. Mailing address: Molecular Immunology, Helmholtz Centre for Infection Research, Inhoffenstraße 7, D-38124 Braunschweig, Germany. Phone: 49 531 6181 5110. Fax: 49 531 6181 5002. E-mail: jja{at}gbf.de.

{triangledown} Published ahead of print on 30 October 2006.

Editor: J. L. Flynn

Infection and Immunity, January 2007, p. 462-470, Vol. 75, No. 1
0019-9567/07/$08.00+0     doi:10.1128/IAI.00443-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Carrero, J. A., Calderon, B., Vivanco-Cid, H., Unanue, E. R. (2009). Recombinant Listeria monocytogenes Expressing a Cell Wall-Associated Listeriolysin O Is Weakly Virulent but Immunogenic. Infect. Immun. 77: 4371-4382 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»