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a poisonous substance produced during the metabolism and growth of certain microorganisms and some higher plant and animal species

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(特にバクテリアの)毒素

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/10/15 11:50:42」(JST)

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Ribbon diagram of Shiga toxin (Stx) from S. dysenteriae. From PDB: 1R4Q.

Shiga toxins are a family of related toxins with two major groups, Stx1 and Stx2, expressed by genes considered to be part of the genome of lambdoid prophages.^[1] The toxins are named for Kiyoshi Shiga, who first described the bacterial origin of dysentery caused by Shigella dysenteriae. The most common sources for Shiga toxin are the bacteria S. dysenteriae and the shigatoxigenic group of Escherichia coli (STEC), which includes serotypes O157:H7, O104:H4, and other enterohemorrhagic E. coli (EHEC).^[2]^[3]

Nomenclature

Microbiologists use many terms to describe Shiga toxin and differentiate more than one unique form. Many of these terms are used interchangeably.

Shiga toxin (Stx) - true Shiga toxin - is produced by Shigella dysenteriae.
Shiga-like toxins 1 and 2 (SLT-1 and 2 or Stx-1 and 2) are the Shiga toxins produced by some E. coli strains. Stx-1 differs from Stx by only one amino acid. Stx-2 shares 56% sequence identity with Stx-1.
Cytotoxins - an archaic denotation for Stx - is used in a broad sense.
Verocytotoxins/verotoxins - a seldom-used term for Stx - is from the hypersensitivity of Vero cells to Stx.

Mechanism

Shiga toxins act to inhibit protein synthesis within target cells by a mechanism similar to that of ricin toxin produced by Ricinus communis.^[4] After entering a cell via a macropinosome,^[5] the protein functions as an N-glycosidase, cleaving a specific adenine nucleobase from the 28S RNA of the 60S subunit of the ribosome, thereby halting protein synthesis.^[6]

Structure

The toxin has two subunits—designated A (mol. wt. 32000 D) and B (mol. wt. 7700 D)—and is one of the AB₅ toxins. The B subunit is a pentamer that binds to specific glycolipids on the host cell, specifically globotriaosylceramide (Gb3). Following this, the A subunit is internalised and cleaved into two parts. The A1 component then binds to the ribosome, disrupting protein synthesis. Stx-2 has been found to be about 400 times more toxic (as quantified by LD₅₀ in mice) than Stx-1.

Gb3 is, for unknown reasons, present in greater amounts in renal epithelial tissues, to which the renal toxicity of Shiga toxin may be attributed. Gb3 is also found in central nervous system neurons and endothelium, which may lead to neurotoxicity.^[7] Stx-2 is also known to increase the expression of its receptor GB3 and cause neuronal dysfunctions.^[8]

The toxin requires highly specific receptors on the cells' surface to attach and enter the cell; species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, shedding them in their feces, from where they may be spread to humans.^[9]

References

^ Friedman D, Court D (2001). "Bacteriophage lambda: alive and well and still doing its thing". Current Opinion in Microbiology 4 (2): 201–7. doi:10.1016/S1369-5274(00)00189-2. PMID 11282477.
^ Beutin L (2006). "Emerging enterohaemorrhagic Escherichia coli, causes and effects of the rise of a human pathogen". J Vet Med B Infect Dis Vet Public Health 53 (7): 299–305. doi:10.1111/j.1439-0450.2006.00968.x. PMID 16930272.
^ Spears; et al. (2006). "A comparison of Enteropathogenic and enterohaemorragic E.coli pathogenesis". FEMS Microbiology Letters: 187–202.
^ Sandvig K, van Deurs B (2000). "Entry of ricin and Shiga toxin into cells: molecular mechanisms and medical perspectives". The EMBO Journal 19 (22): 5943–50. doi:10.1093/emboj/19.22.5943. PMC 305844. PMID 11080141.
^ Lukyanenko, V.; Malyukova, I.; Hubbard, A.; Delannoy, M.; Boedeker, E.; Zhu, C.; Cebotaru, L.; Kovbasnjuk, O. (2011). "Enterohemorrhagic Escherichia coli infection stimulates Shiga toxin 1 macropinocytosis and transcytosis across intestinal epithelial cells". AJP: Cell Physiology 301 (5): C1140–C1149. doi:10.1152/ajpcell.00036.2011. PMC 3213915. PMID 21832249.
^ Sandvig K, Bergan J, Dyve A, Skotland T, Torgersen M.L. (2010). "Endocytosis and retrograde transport of Shiga toxin". Toxicon. 56 Suppl 7: 1181–1185. doi:10.1016/j.toxicon.2009.11.021. PMID 2047652.
^ Obata F, Tohyama K, Bonev AD, Kolling GL, Keepers TR, Gross LK, Nelson MT, Sato S, Obrig TG (2008). "Shiga Toxin 2 Affects the Central Nervous System through Receptor Globotriaosylceramide Localized to Neurons". J Infect Dis 198 (9): 1398–1406. doi:10.1086/591911. PMC 2684825. PMID 18754742.
^ Tironi-Farinati C, Loidl CF, Boccoli J, Parma Y, Fernandez-Miyakawa ME, Goldstein J. (2010). "Intracerebroventricular Shiga toxin 2 increases the expression of its receptor globotriaosylceramide and causes dendritic abnormalities". J Neuroimmunol 222 (1–2): 48–61. doi:10.1016/j.jneuroim.2010.03.001. PMID 20347160.
^ Asakura H, Makino S, Kobori H, Watarai M, Shirahata T, Ikeda T, Takeshi K (2001). "Phylogenetic diversity and similarity of active sites of Shiga toxin (stx) in Shiga toxin-producing Escherichia coli (STEC) isolates from humans and animals". Epidemiol Infect 127 (1): 27–36. doi:10.1017/S0950268801005635. PMC 2869726. PMID 11561972.

External links

Shiga toxin at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

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1. 小児における志賀毒素産生性大腸菌（STEC）溶血性尿毒症症候群（HUS）の臨床症状および診断 clinical manifestations and diagnosis of shiga toxin producing escherichia coli stec hemolytic uremic syndrome hus in children
2. 腸管出血性大腸菌（EHEC）感染症の臨床症状、診断および治療 clinical manifestations diagnosis and treatment of enterohemorrhagic escherichia coli ehec infection
3. 小児における志賀毒素産生性大腸菌（STEC）溶血性尿毒症症候群（HUS）の治療および予後 treatment and prognosis of shiga toxin producing escherichia coli stec hemolytic uremic syndrome hus in children
4. 腸管出血性大腸菌（EHEC）の微生物学、病因、疫学、および予防 microbiology pathogenesis epidemiology and prevention of enterohemorrhagic escherichia coli ehec
5. 小児における溶血性尿毒症症候群の概要 overview of hemolytic uremic syndrome in children

English Journal

Comparison of eight different agars for the recovery of clinically relevant non-O157 Shiga toxin-producing Escherichia coli from baby spinach, cilantro, alfalfa sprouts and raw milk.

Kase JA1, Maounounen-Laasri A2, Son I3, Lin A4, Hammack TS5.
Food microbiology.Food Microbiol.2015 Apr;46:280-7. doi: 10.1016/j.fm.2014.08.020. Epub 2014 Aug 30.
The FDA Bacteriological Analytical Manual (BAM) Chapter 4a recommends several agars for isolating non-O157 Shiga toxin-producing Escherichia coli (STEC); not all have been thoroughly tested for recovering STECs from food. Using E. coli strains representing ten clinically relevant O serogroups (O26,
PMID 25475297

Comparative study on the high pressure inactivation behavior of the Shiga toxin-producing Escherichia coli O104:H4 and O157:H7 outbreak strains and a non-pathogenic surrogate.

Reineke K1, Sevenich R2, Hertwig C3, Janßen T4, Fröhling A3, Knorr D2, Wieler LH4, Schlüter O3.
Food microbiology.Food Microbiol.2015 Apr;46:184-94. doi: 10.1016/j.fm.2014.07.017. Epub 2014 Aug 13.
Enterohemorrhagic Escherichia coli strains cause each year thousands of illnesses, which are sometimes accompanied by the hemolytic uremic syndrome, like in the 2011 outbreak in Germany. For preservation thermal pasteurization is commonly used, which can cause unwanted quality changes. To prevent th
PMID 25475283

The efficacy of short and repeated high-pressure processing treatments on the reduction of non-O157:H7 Shiga-toxin producing Escherichia coli in ground beef patties.

Jiang Y1, Scheinberg JA2, Senevirathne R2, Cutter CN3.
Meat science.Meat Sci.2015 Apr;102:22-6. doi: 10.1016/j.meatsci.2014.12.001. Epub 2014 Dec 5.
High pressure processing (HPP) has previously been shown to be effective at reducing Escherichia coli O157:H7 in meat products. However, few studies have determined whether HPP may be effective at reducing non-O157:H7 Shiga toxin-producing E. coli (STEC) in ground beef. This study investigated the e
PMID 25524823