A report in the January 2007 issue of Nature Immunology explores how shigella bacteria survives and spreads in the gut to cause dysentery -- a severe infection of the gastrointestinal tract that affects millions of people worldwide. The report finds that a protein produced by shigella is injected into host cells and blocks the production of immune signals required for preventing disease.
Laurence Arbibe and colleagues studied Shigella flexneri infection of human colon cells to understand the bacterial factors required to initiate disease. Shigella bacteria are known to inject up to 20 proteins into gut intestinal cells for the purpose of promoting infection and for dampening immune responses.
They found that one of the injected proteins from Shigella flexneri, called OpsF, could prevent gut cells from switching on genes involved in immune responses. As a consequence of OspF function, Shigella flexneri avoids being killed by immune cells of their host and is thus able to spread throughout the gut and cause disease.
This study highlights the precision by which pathogens such as shigella can dramatically alter host cells. It also suggests that blocking OspF may provide a therapeutic target for treating bacterial dysentery that kills hundreds of thousands of people annually.
Laurence Arbibe (Pasteur Institut Paris, France)
Additional comment on the paper:
B. Brett Finlay (University of British Columbia, Vancouver, Canada)
Abstract available online.
(C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza