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Infection and Immunity, February 2005, p. 1069-1080, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.1069-1080.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Murine Macrophage Transcriptional Responses to Bacillus anthracis Infection and Intoxication

Nicholas H. Bergman,1,2 Karla D. Passalacqua,2 Renee Gaspard,3 Lynne M. Shetron-Rama,2 John Quackenbush,3 and Philip C. Hanna2*

Bioinformatics Program,1 Department of Microbiology & Immunology, University of Michigan Medical School, Ann Arbor, Michigan,2 Institute for Genomic Research, Rockville, Maryland3

Received 9 August 2004/ Returned for modification 12 October 2004/ Accepted 29 October 2004

Interactions between Bacillus anthracis and host macrophages represent critical early events in anthrax pathogenesis, but their details are not clearly understood. Here we report the first genomewide characterization of the transcriptional changes within macrophages infected with B. anthracis and the identification of several hundred host genes that were differentially expressed during this intracellular stage of infection. These loci included both genes that are known to be regulated differentially in response to many other bacterial pathogens and those that appear to be differentially regulated in response to B. anthracis but not other bacterial species that have been tested. These data provide a transcriptional basis for a variety of physiological changes observed during infection, including the induction of apoptosis caused by the infecting bacteria. The expression patterns underlying B. anthracis-induced apoptosis led us to test further the importance of one very highly induced macrophage gene, that for ornithine decarboxylase. Our data show that this enzyme plays an important and previously unrecognized role in suppressing apoptosis in B. anthracis-infected cells. We have also characterized the transcriptional response to anthrax lethal toxin in activated macrophages and found that, following toxin treatment, many of the host inflammatory response pathways are dampened. These data provide insights into B. anthracis pathogenesis as well as potential leads for the development of new diagnostic and therapeutic options.

* Corresponding author. Mailing address: Department of Microbiology & Immunology, University of Michigan Medical School, 5641 Med Sci II, Ann Arbor, MI 48109-0620. Phone: (734) 615-3706. Fax: (734) 764-3562. E-mail: pchanna{at}umich.edu.

Editor: D. L. Burns

Infection and Immunity, February 2005, p. 1069-1080, Vol. 73, No. 2
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.2.1069-1080.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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