Shigella flexneri

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Shigella flexneri
Shigella flexneri Gram stain
Scientific classification
Kingdom:Bacteria
Phylum:Proteobacteria
Class:Gamma Proteobacteria
Order:Enterobacteriales
Family:Enterobacteriaceae
Genus:Shigella
Species:S. flexneri
Binomial name
Shigella flexneri
Castellani & Chalmers 1919
 
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Shigella flexneri
Shigella flexneri Gram stain
Scientific classification
Kingdom:Bacteria
Phylum:Proteobacteria
Class:Gamma Proteobacteria
Order:Enterobacteriales
Family:Enterobacteriaceae
Genus:Shigella
Species:S. flexneri
Binomial name
Shigella flexneri
Castellani & Chalmers 1919

Shigella flexneri is a species of Gram-negative bacteria in the genus Shigella that can cause diarrhea in humans. There are several different serogroups of Shigella; S. flexneri belongs to group B. S. flexneri infections can usually be treated with antibiotics although some strains have become resistant. Less severe cases are not usually treated because they become more resistant in the future.[1]

Discovery[edit]

The species was named after the American physician Simon Flexner, in addition to the Japanese physician Kiyoshi Shiga, who researched the cause of dysentery.

Infectious cycle[edit]

S. flexneri contains a virulence plasmid that codes for three virulence factors: a type-3 secretion system (T3SS), invasion plasmid antigen proteins (ipa proteins), and IcsA (used for cell-to-cell spread).[2]

Upon infection, S. flexneri injects the host cell cytoplasm with ipa proteins using the T3SS—a needle-and-syringe like apparatus common to many Gram-negative pathogens. These ipa proteins induce "membrane ruffling" by the host cell. Membrane ruffling creates membrane pockets which capture and engulf the bacteria. Once inside, S. flexneri utilizes host cell actin for propulsion to move directly from cell to cell using a cellular mechanism known as paracytophagy,[3][4] similarly to the bacterial pathogen Listeria monocytogenes.

Recent work has shown that S. flexneri is able to inhibit the acute inflammatory response in the initial stage of infection.[5] It is able to do so by using an effector protein, OspI, which is encoded by ORF169b on the Shigella large plasmid and secreted by the Type III secretion system. It dampens the inflammatory response during bacterial invasion by suppressing the TNF-α-Receptor-associated factor 6 (TRAF6)-mediated signalling pathway.[5] OspI has glutamine deamidase activity, and is able to selectively deaminate glutamine at position 100 in UBC13 to glutamate and this results in a failure of the E2 ubiquitin-conjugating activity which is required for TRAF6 activation.[5]

References[edit]

  1. ^ Ryan KJ, Ray CG, Sherris JC, ed. (2004). Sherris Medical Microbiology (4th ed.). New York: McGraw-Hill. ISBN 978-0-8385-8529-0. LCCN 2003054180. OCLC 52358530. 
  2. ^ Stevens J, Galyov EE, Stevens MP (2006). "Actin-dependent movement of bacterial pathogens". Nature Reviews Microbiology 4 (2): 91–101. doi:10.1038/nrmicro1320. PMID 16415925. 
  3. ^ Ogawa M, Handa Y, Ashida H, Suzuki M, Sasakawa C (2008). "The versatility of Shigella effectors". Nature Reviews Microbiology 6 (1): 11–16. doi:10.1038/nrmicro1814. PMID 18059288. 
  4. ^ Robbins JR, Barth AI, Marquis H, de Hostos EL, Nelson WJ, Theriot JA (1999). "Listeria monocytogenes exploits normal host cell processes to spread from cell to cell". Journal of Cell Biology 146 (6): 1333–1350. doi:10.1083/jcb.146.6.1333. PMC 1785326. PMID 10491395. 
  5. ^ a b c Sanada T, Kim M, Mimuro H, Suzuki M, Ogawa M, Oyama A, Ashida H, Kobayashi T, Koyama T, Nagai S, Shibata Y, Gohda J, Inoue J, Mizushima T, Sasakawa C (2012). "The Shigella flexneri effector OspI deamidates UBC13 to dampen the inflammatory response". Nature 483 (7391): 623–626. doi:10.1038/nature10894. PMID 22407319.