Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Logo for

Science 327 (5964): 417-418

Copyright © 2010 by the American Association for the Advancement of Science

Microbiology

Subversion from the Sidelines

Nisheeth Agarwal, and William R. Bishai

Mycobacterium tuberculosis, which kills 1.7 million people annually, is a pathogen that proliferates within macrophages of the immune system. The granuloma—the hallmark lesion of tuberculosis—forms from repeated waves of macrophages that arrive at the site of infection to combat the pathogen, only to be themselves infected by bacteria multiplying within their dying predecessors. A central tenet in the characterization of tuberculosis has been that the granuloma represents a host defense response that contains the infection. But could the beneficiary of granuloma formation be the pathogen itself rather than the host? On page 466 in this issue, Volkman et al. show that a secreted bacterial peptide and secreted host cell protein are key to stimulating early granuloma development and maintaining the infection (1). The simplest interpretation is that the pathway constitutes a deliberate pro-granulomatous virulence mechanism that benefits the bacteria.

Center for Tuberculosis Research, Department of Medicine, Division of Infectious Diseases, Johns Hopkins School of Medicine, Baltimore, MD 21231–1044, USA.

E-mail: wbishai{at}jhmi.edu


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Matrix metalloproteinases in tuberculosis.
P. T. Elkington, C. A. Ugarte-Gil, and J. S. Friedland (2011)
Eur. Respir. J. 38, 456-464
   Abstract »    Full Text »    PDF »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882