Salmonella typhimurium

A Microbial Biorealm page on the genus Salmonella typhimurium

Classification

Higher order taxa

Bacteria; Domain; Proteobacteria; Gammaproteobacteria; Enterobacteriales; Enterobacteriaceae [10]

Species

Salmonella typhimurium

Synonyms: Salmonella choleraesuis serotype typhimurium; Salmonella typhi-murium; Bacillus typhimurium; Salmonella typhi-murium [10]

Description and significance

Salmonella typhimurium is a pathogenic Gram-negative bacteria predominately found in the intestinal lumen. Its toxicity is due to an outer membrane consisting largely of lipopolysaccharides (LPS) which protect the bacteria from the environment. The LPS is made up of an O-antigen, a polysaccharide core, and lipid A, which connects it to the outer membrane. Lipid A is made up of two phosphorylated glucosamines which are attached to fatty acids. These phosphate groups determine bacterial toxicity. Animals carry an enzyme that specifically removes these phosphate groups in an attempt to protect themselves from these pathogens[4]. The O-antigen, being on the outermost part of the LPS complex is responsible for the host immune response. S. typhimurium has the ability to undergo acetylation of this O-antigen, which changes its conformation, and makes it difficult for antibodies to recognize [5].

Genome structure

A complete genome sequence of Salmonella typhimurium has revealed a chromosome that is 4,857 kilobases long and a virulence plasmid that is 94 kilobases long [12].

Cell structure and metabolism

S. Typhimurium are able to secrete small signaling molecules called autoinducers. The LuxS gene is responsible for initiating a series of phosphate transfer reactions that produce this molecule and allow for cell to cell communication. Sugar compounds, preferably glucose, activate LuxS and the resulting autoinducer concentration increases with the bacterial concentration till the substrate is depleted. At this point the autoinducer is degraded and can be recycled by the bacterial cell. This quorum sensing allows cells to determine the metabolic potential of the environment [1][2].

Ecology

Salmonella typhimurium infect by coming in direct contact with nonphagocytic cells. This contact induces the formation of appendages on the bacterial cell surface. The appendages formed are shorter than flagella but thicker than both flagella and pili. They cause the host cytoskeleton to rearrange which allows the bacteria to enter the cell. This membrane ruffling system is due to 14 genes at 58-60 minutes on the S. typhimurium chromosome. The inv genes located at 59 minutes are responsible for the assemblage and emission/withdrawal of these appendages. All of the inv genes must be intact for this system to work. One of these genes, invC, is responsible for ATPase which provides the energy needed to complete this ruffling process [11].

Pathology

Salmonella typhimurium causes gastroenteritis in humans and other mammals. When the bacterial cells enter epithelial cells lining the intestine they cause host cell ruffling which temporarily damages the microvilli on the surface of the cell. This causes a rush of white blood cells into the mucosa, which throws off the ratios between absorption and secretion, and leads to diarrhea. In mice S. typhimurium causes symptoms resembling typhoid fever in humans. Studying these bacteria in mice could eventually lead to a typhoid vaccine [7][8][9].

Application to Biotechnology

Salmonella typhimurium has been used to investigate its ability to deliver DNA to antigen presenting cells (APCs) in order to produce cancer vaccines. Studies indicate that S. typhimurium has been able to initiate an immune response as a direct result of the DNA containing “eukaryotic expression vectors.” Hopefully these experiments will lead to the ability to send specific DNA sequences that will illicit the appropriate immune response to eliminate tumor or cancer cells [13].

Current Research

Mice exhibit typhoid like symptoms when infected with Salmonella typhimurium and are currently being used to develop a typhoid vaccine [9].

References

1. Winzer, Klaus, et al. "LuxS: its role in central metabolism and the in vitro synthesis of 4-hydroxy-5-methyl-3(2H)-furanone." Microbiology (2002): 909-922. Microbiology. 2007. Society for General Microbiology. 5 June 2007 <http://mic.sgmjournals.org/cgi/content/full/148/4/909?ck=nck#SEC3>.

2. Surette, Michael G., and Bonnie L. Bassler. "Quorum sensing in Escherichia coli and Salmonella typhmurium." Microbiology 95.7046–7050 (June 1998): 12. Proceedings of the National Academy of Sciences of the United States of America. 2007. National Academy of Sciences. 5 June 2007 <http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=22733>.

3. Ahmer, Brian, et al. "Salmonella typhimurium Encodes an SdiA Homolog, a Putative Quorum Sensor of the LuxR Family, That Regulates Genes on the Virulence Plasmid." Journal of Bacteriology 180.5 (Mar. 1998): 1185-1193. Journal of Bacteriology. 2007. American Society for Microbiology. 5 June 2007 <http://jb.asm.org/cgi/content/full/180/5/1185>.

4. Tuin, Annemarie, et al. "On the role and fate of LPS-dephosphorylating activity in the rat liver." American Journal of Physiology- Gastrointestinal and Liver Physiology 290 (Oct. 2005): G377-G385. American Journal of Physiology- Gastrointestinal and Liver Physiology. 2006. American Physiological Society. 5 June 2007 <http://ajpgi.physiology.org/cgi/content/full/290/2/G377#T1>.

5. Slauch, James, et al. "Acetylation (O-Factor 5) Affects the Structural and Immunological." Infection and Immunity 63.2 (Feb. 1995): 437-441. Infection and Immunity. 5 June 2007. American Society for Microbiology. 5 June 2007 <http://iai.asm.org/cgi/reprint/63/2/437>.

6. Garcia-Del Portillo, Francisco, Murray Stein, and B Finlay. "Release of Lipopolysaccharide from Intracellular Compartments." Infection and Immunity 65.1 (Jan. 1997): 24-34. Infection and Immunity. 5 June 2007. American Society for Microbiology. 5 June 2007 <http://iai.asm.org/cgi/reprint/65/1/24>.

7. McCormick, Beth, et al. "Transepithelial Signaling to Neutrophils by Salmonellae: a Novel." Infection and Immunity 63.6 (June 1995): 2302-2309. Infection and Immunity. 5 June 2007. American Society for Microbiology. 5 June 2007 <http://iai.asm.org/cgi/reprint/63/6/2302>.

8. Miao, Edward, et al. "Salmonella typhimurium leucine-rich repeat." Molecular Microbiology 34.4 (1999): 850-864. Blackwell Synergy. 1999. 5 June 2007 <http://www.blackwell-synergy.com/links/doi/10.1046/j.1365-2958.1999.01651.x/pdf>.

9. Everest, Paul, et al. "Evaluation of Salmonella typhimurium Mutants in a Model of Experimental Gastroenteritis." Infection and Immunity 67.6 (June 1999): 2815-2821. Infection and Immunity. 2007. American Society for Microbiology. 5 June 2007 <http://iai.highwire.org/cgi/content/full/67/6/2815>.

10."Salmonella typhimurium." Taxonomy Browser. Ed. Joe Bischoff, et al. 10 Jan. 2007. NCBI. 3 May 2007 <http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=602&lvl=3&p=mapview&p=has_linkout&p=blast_url&p=genome_blast&lin=f&keep=1&srchmode=1&unlock>.

11. Ginocchio, Christine, et al. "Contact with epithelial cells induces the formation of surface appendages on Salmonella typhimurium." Cell 76.4 (Feb. 1994): 717-724. Science Direct. 2007. Elsevier. 3 June 2007 <http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WSN-4C6BNSY-DP&_user=10&_coverDate=02%2F25%2F1994&_rdoc=1&_fmt=summary&_orig=browse&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=e35aee64c97ab33b4f23f0371633e4e0>.

12. McClelland, M, and KE Sanderson. "PubMed." NCBI. 2007. Department of Health and Human Services. 5 June 2007 <http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11677609>.

Edited by Janela Aitchison student of Dr. Rachel Larsen and Dr. Kit Pogliano