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Infection and Immunity, November 2006, p. 6449-6457, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00190-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Regulation of Mycobacterium tuberculosis whiB3 in the Mouse Lung and Macrophages{triangledown}

N. Banaiee,1* W. R. Jacobs Jr.,2 and J. D. Ernst1,3

Division of Infectious Diseases, Department of Medicine,1 Department of Microbiology, New York University School of Medicine, New York, New York 10016,3 Howard Hughes Medical Institute and Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 104612

Received 2 February 2006/ Returned for modification 29 March 2006/ Accepted 7 August 2006

Mycobacterium tuberculosis is a highly successful human pathogen, with ~2 x 109 individuals infected globally. To understand the responses of M. tuberculosis to the in vivo environment, we studied the in vivo regulation of M. tuberculosis genes whose M. marinum homologs are induced in chronically infected frog tissues. The expression of 16S rRNA was shown to remain constant in M. tuberculosis under in vivo and in vitro conditions and therefore could be used for internal normalization in quantitative reverse transcription-PCR assays. We found whiB3, a putative transcriptional regulator implicated in mediating tissue damage, to be maximally induced at 2 weeks postinfection in the lungs of wild-type and immunodeficient (gamma interferon receptor–/–, Rag1–/–, and tumor necrosis factor alpha–/–) mice. At later time points in wild-type mice, whiB3 induction was decreased and gradually declined over the course of infection. In immunodeficient mice, whiB3 induction declined rapidly and was completely abolished in moribund animals. whiB3 was also found to be induced in naïve bone marrow-derived macrophages after 6 h of infection. whiB3 expression in vivo and in vitro was found to be inversely correlated with bacterial density. These results indicate that M. tuberculosis regulates the expression of whiB3 in response to environmental signals present in vivo and are consistent with a model of regulation by quorum sensing.

* Corresponding author. Mailing address: New York University School of Medicine, Smilow Research Center, 522 First Avenue, SML 901, New York, NY 10016. Phone: (212) 263-6785. Fax: (212) 263-7749. E-mail: banain01{at}med.nyu.edu.

{triangledown} Published ahead of print on 21 August 2006.

Editor: J. L. Flynn

Infection and Immunity, November 2006, p. 6449-6457, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00190-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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