Clostridium perfringens Alpha-toxin Recognizes the GM1a-TrkA Complex

Oda, Masataka; Kabura, Michiko; Takagishi, Teruhisa; Suzue, Ayaka; Tominaga, Kaori; Urano, Shiori; Nagahama, Masahiro; Kobayashi, Kazuo; Furukawa, Koichi; Sakùrai, Jun

doi:10.1074/jbc.m112.393801

Cited by 43 publications

(46 citation statements)

References 51 publications

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“…Therefore, direct disruption of the host cell membrane is not the only mechanism by which CPA causes cell lysis. It has also been shown that CPA activates the MEK/extracellular signal-regulated kinase (ERK) pathway and thereby induces oxidative stress in affected cells (36,37) and interleukin-8 (IL-8) production by stimulating both the ERK1/2 and p38 mitogen-activated protein kinase (MAPK) pathways (38). Recent studies suggested that CPA may induce signal transduction changes after binding to a ganglioside GM1 receptor (38).…”

Section: Chromosomally Encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

226

282

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SUMMARY In both humans and animals, Clostridium perfringens is an important cause of histotoxic infections and diseases originating in the intestines, such as enteritis and enterotoxemia. The virulence of this Gram-positive, anaerobic bacterium is heavily dependent upon its prolific toxin-producing ability. Many of the ∼16 toxins produced by C. perfringens are encoded by large plasmids that range in size from ∼45 kb to ∼140 kb. These plasmid-encoded toxins are often closely associated with mobile elements. A C. perfringens strain can carry up to three different toxin plasmids, with a single plasmid carrying up to three distinct toxin genes. Molecular Koch's postulate analyses have established the importance of several plasmid-encoded toxins when C. perfringens disease strains cause enteritis or enterotoxemias. Many toxin plasmids are closely related, suggesting a common evolutionary origin. In particular, most toxin plasmids and some antibiotic resistance plasmids of C. perfringens share an ∼35-kb region containing a Tn 916 -related conjugation locus named tcp (transfer of clostridial plasmids). This tcp locus can mediate highly efficient conjugative transfer of these toxin or resistance plasmids. For example, conjugative transfer of a toxin plasmid from an infecting strain to C. perfringens normal intestinal flora strains may help to amplify and prolong an infection. Therefore, the presence of toxin genes on conjugative plasmids, particularly in association with insertion sequences that may mobilize these toxin genes, likely provides C. perfringens with considerable virulence plasticity and adaptability when it causes diseases originating in the gastrointestinal tract.

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Section: Chromosomally Encoded Toxinsmentioning

confidence: 99%

Toxin Plasmids of Clostridium perfringens

Adams

Bannam

et al. 2013

Microbiol Mol Biol Rev

226

282

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“…However, we have no answer to this proposition, because no solid surface covered by a single SO has been available. Recently, a plastics company developed sugar arrays to search for the binding targets of pathogenic factors (27,28).In the present study, we examined the binding and the gliding of M. mobile on plastic surfaces covered by uniform oligosaccharides, and concluded that the variations in sugar structures cause …”

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confidence: 99%

Gliding Motility of Mycoplasma mobile on Uniform Oligosaccharides

2015

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The binding and gliding of Mycoplasma mobile on a plastic plate covered by 53 uniform oligosaccharides were analyzed. Mycoplasmas bound to and glided on only 21 of the fixed sialylated oligosaccharides (SOs), showing that sialic acid is essential as the binding target. The affinities were mostly consistent with our previous results on the inhibitory effects of free SOs and suggested that M. mobile recognizes SOs from the nonreducing end with four continuous sites as follows. (i and ii) A sialic acid at the nonreducing end is tightly recognized by tandemly connected two sites. (iii) The third site is recognized by a loose groove that may be affected by branches. (iv) The fourth site is recognized by a large groove that may be enhanced by branches, especially those with a negative charge. The cells glided on uniform SOs in manners apparently similar to those of the gliding on mixed SOs. The gliding speed was related inversely to the mycoplasma's affinity for SO, suggesting that the detaching step may be one of the speed determinants. The cells glided faster and with smaller fluctuations on the uniform SOs than on the mixtures, suggesting that the drag caused by the variation in SOs influences gliding behaviors. IMPORTANCEMycoplasma is a group of bacteria generally parasitic to animals and plants. Some Mycoplasma species form a protrusion at a pole, bind to solid surfaces, and glide in the direction of the protrusion. These procedures are essential for parasitism. Usually, mycoplasmas glide on mixed sialylated oligosaccharides (SOs) derived from glycoprotein and glycolipid. Since gliding motility on uniform oligosaccharides has never been observed, this study gives critical information about recognition and interaction between receptors and SOs. M ycoplasmas are parasitic and occasionally commensal bacteria that have small genomes and lack a peptidoglycan layer (1). Several Mycoplasma species form membrane protrusions, such as the headlike structure in Mycoplasma mobile (2) and the attachment organelle in the human pathogen Mycoplasma pneumoniae (3-5). On solid surfaces, these species exhibit gliding motility in the direction of the protrusion; this motility appears to be involved in the parasitism of mycoplasmas. Interestingly, mycoplasmas have no flagella or pili, and their genomes contain no genes related to known bacterial motility. In addition, no homologs of motor proteins that are common in eukaryotic motility have been found.M. mobile, isolated from the gills of freshwater fish, is a fastgliding mycoplasma. It glides smoothly and continuously on glass at an average speed of 2.0 to 4.5 m/s (6, 7), or three to seven times the length of the cell per second, exerting a force of up to 27 pN (8-10). The gliding machinery formed at the base of the membrane protrusion can be divided into internal and surface structures. The internal, "jellyfish" structure is composed of about 10 proteins (11, 12). The surface structure is composed of hundreds of units, with a flexible leg protruding from each (13-15). The l...

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“…In addition to disrupting membrane phospholipids through phospholipase activity, α-toxin binding to GM1a triggers specific signaling events. The activation of a tyrosine kinase A (TrkA) [45] and the subsequent signaling cascade results in the release of tumor necrosis factor-α (TNF-α). The catastrophic events induced by α-toxin may in part be mediated by TNF-α signaling.…”

Section: Discussionmentioning

confidence: 99%

Gas-forming liver abscess associated with rapid hemolysis in a diabetic patient

Kurasawa¹,

Nishikido²,

Koike³

et al. 2014

WJD

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We experienced a case of liver abscess due to Clostridium perfringens (CP ) complicated with massive hemolysis and rapid death in an adequately controlled type 2 diabetic patient. The patient died 6 h after his first visit to the hospital. CP was later detected in a blood culture. We searched for case reports of CP septicemia and found 124 cases. Fifty patients survived, and 74 died. Of the 30 patients with liver abscess, only 3 cases survived following treatment with emergency surgical drainage. For the early detection of CP infection, detection of Gram-positive rods in the blood or drainage fluid is important. Spherocytes and ghost cells indicate intravascular hemolysis. The prognosis is very poor once massive hemolysis occurs. The major causative organisms of gas-forming liver abscess in diabetic patients are Klebsiella pneumoniae (K. pneumoniae ) and Escherichia coli (E. coli ). Although CP is relatively rare, the survival rate is very poor compared with those of K. pneumoniae and E. coli . Therefore, for every case that presents with a gas-forming liver abscess, the possibility of CP should be considered, and immediate aspiration of the abscess and Gram staining are important.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Liver abscess; Gas-forming; Clostridium perfringens ; Hemolysis; Diabetes Core tip: Gas-forming liver abscess caused by Clostridium perfringens can result in massive hemolysis and death within several hours. For survival, urgent surgical intervention and antibiotic administration are necessary.Kurasawa M, Nishikido T, Koike J, Tominaga S, Tamemoto H. Gas-forming liver abscess associated with rapid hemolysis in a diabetic patient. World J Diabetes 2014; 5(2): 224-229 Available from:

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Clostridium perfringens Alpha-toxin Recognizes the GM1a-TrkA Complex

Cited by 43 publications

References 51 publications

Toxin Plasmids of Clostridium perfringens

Toxin Plasmids of Clostridium perfringens

Gliding Motility of Mycoplasma mobile on Uniform Oligosaccharides

Gas-forming liver abscess associated with rapid hemolysis in a diabetic patient

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