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Molecular and Cellular Biology, January 2003, p. 526-533, Vol. 23, No. 2
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.2.526-533.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Regulation of Tumor Necrosis Factor Alpha Gene Expression by Mycobacteria Involves the Assembly of a Unique Enhanceosome Dependent on the Coactivator Proteins CBP/p300

Robert Barthel,1 Alla V. Tsytsykova,1 Amy K. Barczak,1 Eunice Y. Tsai,1 Christopher C. Dascher,2,3 Michael B. Brenner,2,3 and Anne E. Goldfeld1,2*

The Center for Blood Research,1 Department of Medicine, Harvard Medical School,2 The Brigham and Women's Hospital, Boston, Massachusetts 021153

Received 11 September 2002/ Returned for modification 14 October 2002/ Accepted 18 October 2002

Tumor necrosis factor alpha (TNF-{alpha}) plays an important role in host containment of infection by Mycobacterium tuberculosis, one of the leading causes of death by an infectious agent globally. Using the pathogenic M. tuberculosis strain H37Rv, we present evidence that upon stimulation of monocytic cells by M. tuberculosis a unique TNF-{alpha} enhanceosome is formed, and it is distinct from the TNF-{alpha} enhanceosome that forms in T cells stimulated by antigen engagement or virus infection. A distinct set of activators including ATF-2, c-jun, Ets, Sp1, Egr-1 and the coactivator proteins CBP/p300 are recruited to the TNF-{alpha} promoter after stimulation with M. tuberculosis. Furthermore, the formation of this enhanceosome is dependent on inducer-specific helical phasing relationships between transcription factor binding sites. We also show that the transcriptional activity of CBP/p300 is potentiated by mycobacterial stimulation of monocytes. The identification of TNF-{alpha} regulatory elements and coactivators involved in M. tuberculosis-stimulated gene expression thus provides potential selective molecular targets in the modulation of TNF-{alpha} gene expression in the setting of mycobacterial infection.

* Corresponding author. Mailing address: Center for Blood Research, 800 Huntington Ave., Boston, MA 02115. Phone: (617) 278-3351. Fax: (617) 278-3454. E-mail: goldfeld{at}cbr.med.harvard.edu.

Molecular and Cellular Biology, January 2003, p. 526-533, Vol. 23, No. 2
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.2.526-533.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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