Components of the peptidoglycan-recycling pathway modulate invasion and intracellular survival of Salmonella enterica serovar Typhimurium

Authors: Anders Folkesson¹; Sofia Eriksson¹; Mats Andersson¹; James T. Park²; Staffan Normark¹

Source: Cellular Microbiology, Volume 7, Number 1, January 2005 , pp. 147-155(9)

Buy & download fulltext article:

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

Please click here to view this article on Wiley Online Library.

You may be required to register and activate access on Wiley Online Library before you can obtain the full text. If you have any queries please visit Wiley Online Library

Abstract:

Summary

-Lactam resistance in enteric bacteria is frequently caused by mutations in ampD encoding a cytosolic N-acetylmuramyl-l-alanine amidase. Such mutants are blocked in murein (peptidoglycan) recycling and accumulate cytoplasmic muropeptides that interact with the transcriptional activator ampR, which de-represses bgr

-lactamase expression. Salmonella enterica serovar Typhimurium, an extensively studied enteric pathogen, was used to show that mutations in ampD decreased the ability of S. typhimurium to enter a macrophage derived cell line and made the bacteria more potent as inducers of inducible nitric oxide synthase (iNOS), as compared with the wild-type. ampG mutants, defective in the transport of recycled muropeptides across the cytoplasmic membrane, behaved essentially as the wild-type in invasion assays and in activation of iNOS. As ampD mutants also have reduced in vivo fitness in a murine model, we suggest that the cytoplasmic accumulation of muropeptides affects the virulence of the ampD mutants.

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1462-5822.2004.00443.x

Affiliations: 1: Mikrobiologiskt och Tumörbiologiskt Centrum, Karolinska Institutet, S-17177 Stockholm, Sverige, Sweden. 2: Department of Molecular Biology and Microbiology, Tufts University, Boston, MA 02111, USA.

Publication date: 2005-01-01