IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 Howe, D.
Right arrow Articles by Mallavia, L. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Howe, D.
Right arrow Articles by Mallavia, L. P.

 Previous Article  |  Next Article 

Infection and Immunity, July 1999, p. 3236-3241, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Coxiella burnetii Infection Increases Transferrin Receptors on J774A.1 Cellsdagger

Dale Howe,* and Louis P. Mallavia

Department of Microbiology, Washington State University, Pullman, Washington 99164-4233

Received 25 November 1998/Returned for modification 20 January 1999/Accepted 3 March 1999

Inoculation with viable, but not inactivated, Coxiella burnetii resulted in the increased expression of transferrin receptors (TfR) in the murine macrophage-like cell line J774A.1. This upregulation was evident in immunoblots as early as 6 h postinfection, with TfR levels continuing to increase through the first 24 h of infection. Fluorescent labeling revealed that TfR upregulation occurred throughout infected monolayers, eliminating the possibility that it reflected a response by a minor subset of host cells. In addition, TfR trafficking did not appear to be affected by C. burnetii infection. Consistent with the increase in TfRs, inoculation with viable C. burnetii resulted in a 2.5-fold increase in total cellular iron by 12 h postinoculation. Our further findings that the chelation of intracellular iron arrests C. burnetii replication and that C. burnetii metabolic activities in vitro are affected by iron concentration suggest that TfR upregulation is a salient factor in C. burnetii infection, and we speculate that it may represent a significant virulence mechanism.


* Corresponding author. Mailing address: University of Wyoming, Department of Molecular Biology, Laramie, WY 82071-3944. Phone: (307) 766-3435. Fax: (307) 766-5098. E-mail: dhowe{at}uwyo.edu.

dagger This paper is dedicated to the memory of Louis P. Mallavia.


Infection and Immunity, July 1999, p. 3236-3241, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 1999 by the American Society for Microbiology. All rights reserved.