IngentaConnect The Salmonella SPI1 effector SopB stimulates nitric oxide product...

Authors: Dan Drecktrah¹; Leigh A. Knodler¹; Kendal Galbraith¹; Olivia Steele-Mortimer

Source: Cellular Microbiology, Volume 7, Number 1, January 2005 , pp. 105-113(9)

Abstract:

Summary

The ability of Salmonella enterica to invade and replicate within host cells depends on two type III secretion systems (TTSSs) encoded on pathogenicity islands 1 and 2 (SPI1 and SPI2). The current paradigm holds that these systems translocate two classes of effectors that operate sequentially and independently. In essence, the SPI1 TTSS mediates early events (i.e. invasion) whereas the SPI2 TTSS mediates post-invasion processes (i.e. replication, vacuole maturation). Contrary to this model, we have found in infected macrophages that a SPI1 effector, SopB/SigD, increased inducible nitric oxide synthase levels and nitric oxide production, host cell process previously known only to be a target of the SPI2 TTSS. Furthermore, SopB protein and message persist many hours after invasion. Our findings reveal an unanticipated potential for dialogue between the SPI1 and SPI2 TTSS and the host cell response.

Document Type: Research article

DOI: 10.1111/j.1462-5822.2004.00436.x

Affiliations: 1: Laboratory of Intracellular Parasites, National Institutes of Allergy and Infectious Diseases, Rocky Mountain Laboratories, Hamilton, MT 59840, USA.

You have access to the full text article on a website external to Ingentaconnect.

Please click here to view this article on InterScience.

You may be required to register and activate access on InterScience before you can obtain the full text. If you have any queries please contact onlinehelp@oxon.blackwellpublishing.com

The Salmonella SPI1 effector SopB stimulates nitric oxide production long after invasion