Present addresses: Jay C.D. Hinton, Department of Microbiology, School of Genetics and Microbiology, Moyne Institute of Preventive Medicine, Trinity College, Dublin 2, Ireland. Edouard E. Galyov, Department of Infection, Immunity & Inflammation, Maurice Shock Building, University of Leicester, PO Box 138, Leicester LE1 9HN, UK.
Salicylidene acylhydrazide-mediated inhibition of type III secretion system-1 in Salmonella enterica serovar Typhimurium is associated with iron restriction and can be reversed by free iron
Article first published online: 6 NOV 2009
© 2009 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Microbiology Letters
Volume 302, Issue 2, pages 114–122, January 2010
How to Cite
Layton, A. N., Hudson, D. L., Thompson, A., Hinton, J. C.D., Stevens, J. M., Galyov, E. E. and Stevens, M. P. (2010), Salicylidene acylhydrazide-mediated inhibition of type III secretion system-1 in Salmonella enterica serovar Typhimurium is associated with iron restriction and can be reversed by free iron. FEMS Microbiology Letters, 302: 114–122. doi: 10.1111/j.1574-6968.2009.01847.x
Editor: Rob Delahay
- Issue published online: 16 DEC 2009
- Article first published online: 6 NOV 2009
- Received 26 August 2009; accepted 16 October 2009.Final version published online 27 November 2009.
- type III secretion;
- salicylidene acylhydrazide;
Salmonella enterica serovar Typhimurium is an animal and zoonotic pathogen of worldwide importance. Intestinal colonization, induction of enteritis and systemic translocation by this bacterium requires type III protein secretion. Strategies that target this process have the potential to control infection, pathology and transmission. We defined the global transcriptional response of S. Typhimurium to INP0403, a member of a family of salicylidene acylhydrazides that inhibit type III secretion (T3S). INP0403 treatment was associated with reduced transcription of genes involved in T3S, but also increased transcription of genes associated with iron acquisition. We show that INP0403 restricts iron availability to Salmonella, and that inhibition of T3S system-1 by INP0403 is, at least in part, reversible by exogenous iron and independent of the iron response regulator Fur.