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Infection and Immunity, July 1999, p. 3236-3241, Vol. 67, No. 7
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.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Coxiella burnetii Infection Increases
Transferrin Receptors on J774A.1 Cells
*
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.
This paper is dedicated to the memory of Louis P. Mallavia.
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