The Salmonella SPI1 effector SopB stimulates nitric oxide production long after invasion
Article first published online: 4 AUG 2004
Volume 7, Issue 1, pages 105–113, January 2005
How to Cite
Drecktrah, D., Knodler, L. A., Galbraith, K. and Steele-Mortimer, O. (2005), The Salmonella SPI1 effector SopB stimulates nitric oxide production long after invasion. Cellular Microbiology, 7: 105–113. doi: 10.1111/j.1462-5822.2004.00436.x
- Issue published online: 4 AUG 2004
- Article first published online: 4 AUG 2004
- Received 28 April, 2004; revised 18 May, 2004; accepted 14 June, 2004.
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.