Superantigenic activity of toxic shock syndrome toxin-1 is resistant to heating and digestive enzymes

Li, S.-J.; Hu, Dong‐Liang; Maina, Edward K.; Shinagawa, Kunihiro; Omoe, Katsuhiko; Nakane, Akio

doi:10.1111/j.1365-2672.2010.04927.x

Cited by 26 publications

(30 citation statements)

References 38 publications

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“…However, SElY was unstable in response to digestive enzymes and heat treatment. This property is different from that of other SEs because SEs are well-known to resist heating and digestive enzymes (23). From a phylogenetic tree analysis, SElY was found to be closely related to TSST-1 and SSLs rather than to other SEs.…”

Section: Discussionmentioning

confidence: 81%

“…Three types of protein stability assays were performed as reported previously (23). Bovine serum albumin (BSA; Sigma, St. Louis, MO) was used as a protein control.…”

Section: Methodsmentioning

confidence: 99%

“…Each protein at a concentration of 100 g/ml was incubated with pepsin (100 g/ml) in a final volume of 500 l of 0.1 M sodium acetate buffer (pH 4.5) at 37°C (23). After incubation for the desired periods of time, tubes were removed.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Identification and Characterization of a Novel Staphylococcal Emetic Toxin

Ono

Sato’o

Narita

et al. 2015

Appl Environ Microbiol

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e Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus have superantigenic and emetic activities, which cause toxic shock syndrome and staphylococcal food poisoning, respectively. Our previous study demonstrated that the sequence of SET has a low level of similarity to the sequences of other SEs and exhibits atypical bioactivities. Hence, we further explored whether there is an additional SET-related gene in S. aureus strains. One SET-like gene was found in the genome of S. aureus isolates that originated from a case of food poisoning, a human nasal swab, and a case of bovine mastitis. The deduced amino acid sequence of the SET-like gene showed 32% identity with the amino acid sequence of SET. The SET-like gene product was designated SElY. In the food poisoning and nasal swab isolates, mRNA encoding SElY was highly expressed in the early log phase of cultivation, whereas a high level of expression of this mRNA was found in the bovine mastitis isolate at the early stationary phase. To estimate whether SElY has both superantigenic and emetic activities, recombinant SElY was prepared. Cell proliferation and cytokine production were examined to assess the superantigenic activity of SElY. SElY exhibited superantigenic activity in human peripheral blood mononuclear cells but not in mouse splenocytes. In addition, SElY exhibited emetic activity in house musk shrews after intraperitoneal and oral administration. However, the stability of SElY against heating and pepsin and trypsin digestion was different from that of SET and SEA. From these results, we identified SElY to be a novel staphylococcal emetic toxin. Staphylococcus aureus produces a variety of exotoxins, including staphylococcal enterotoxins (SEs) and toxic shock syndrome toxin 1 (TSST-1) (1). These toxins are superantigens, which have the ability to stimulate a large repertoire of the V␤ elements of T cell receptor (TCR)-bearing T cells. SEs are also emetic toxins causing staphylococcal food poisoning in humans, although the mechanism of SE-induced emesis has not been entirely verified (2). Due to these properties, SEs are assumed to be a menace to public health. Five major serological types (SEA to SEE) have been characterized (2), and new types of SE-related toxins (SEG to SEI, SElJ, SEK to SET, SElU, SElV, and SElX) have recently been reported (2-8). Moreover, superantigen-related genes, such as staphylococcal superantigen-like protein (SSL) genes (ssl1 to ssl26), were discovered during determination of the complete genome sequences of several S. aureus strains (9-11). It has been recognized that the superantigen genes are associated with mobile genetic elements (MGEs), such as pathogenicity islands, prophages, or plasmids (5,(11)(12)(13)(14). This fact implies that these superantigen genes move among S. aureus strains by horizontal transfer and that such MGEs play an important role in the evolution of S. aureus as a pathogen.We have reported that SET shows mitogenicity to human T cells and requires major histocompatibility complex (MHC) cla...

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Section: Discussionmentioning

confidence: 81%

“…Three types of protein stability assays were performed as reported previously (23). Bovine serum albumin (BSA; Sigma, St. Louis, MO) was used as a protein control.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Identification and Characterization of a Novel Staphylococcal Emetic Toxin

Ono

Sato’o

Narita

et al. 2015

Appl Environ Microbiol

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“…In 1930, it was shown that this food poisoning was not caused from infection by Staphylococcus aureus but from intoxication by a heatstable exotoxin (later termed an 'enterotoxin') produced by the bacterium in contaminated foods (Dack et al, 1930). SEs are singlechain, heat-stable proteins that are 23-27 kDa in size and are resistant to proteolytic enzymes (Balaban & Rasooly, 2000;Li et al, 2011). Today, staphylococcal enterotoxins (SEs) are recognized as the most common causative agents of human food poisoning worldwide (Kotb, 1995;Balaban & Rasooly, 2000).…”

Section: Introductionmentioning

confidence: 99%

Submucosal mast cells in the gastrointestinal tract are a target of staphylococcal enterotoxin type A

Ono

Nishizawa

Yamamoto

et al. 2012

FEMS Immunol Med Microbiol

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Staphylococcal enterotoxin A (SEA) is a leading causative toxin of staphylococcal food poisoning. However, it remains unclear how this toxin induces emesis in humans, primates, and certain experimental animals. To understand the mechanism of SEA-induced emesis, we investigated the behavior of SEA in the gastrointestinal (GI) tract in vivo using the house musk shrew (Suncus murinus). Immunofluorescence of GI sections showed that perorally administered SEA translocated from the lumen to the interior tissues of the GI tract and rapidly accumulated in certain submucosa cells. These SEA-binding cells in the submucosa were both tryptase- and FcεRIα-positive, suggesting these SEA-binding cells were mast cells. These SEA-binding mast cells were 5-hydroxytryptamine (5-HT)-positive, but the intensity of the 5-HT signal decreased over time compared to that of mast cells in the negative control. Furthermore, toluidine blue staining showed the number of metachromatic mast cells was decreased in the duodenal submucosa, suggesting that SEA binding induced degranulation and release of 5-HT from submucosal mast cells. These observations suggest that the target cells of SEA are submucosal mast cells in the GI tract and that 5-HT released from submucosal mast cells plays an important role in SEA-induced emesis.

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“…It is still unclear why these two superantigenic toxins (SE and TSST-1) show different pathogenesis in infections and food poisoning induced by S. aureus. Research study conducted by Li et al (2011) showed strong resistance of the superantigenic activity of TSST-1 to heat treatment, pepsin and trypsin digestion. Although TSST-1 was rapidly degraded to smaller fragments after treatment with pepsin or trypsin, they retained significant superantigenic and lethal shock activities relative to those of SEA.…”

Section: Introductionmentioning

confidence: 99%

Expression of toxic shock syndrome toxin-1 gene of Staphylococcus aureus in milk: Proof of concept

et al. 2018

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The aim of this study was to assess the expression of a toxic shock syndrome toxin-1 (TSST-1) gene of Staphylococcus aureus in different types of milk, depending on inadequate temperature and storage conditions. Pasteurized and UHT milk were inoculated with monotoxic TSST-1 strain of S. aureus and growth kinetics was determined by the drop plate method using Baird-Parker agar medium in accordance with EN ISO 6888-1. The patterns of gene regulation were detected by quantitative reverse transcriptase PCR. Relative quantification method for statistical significance testing was used to detect significant gene expression responses. The results of experiments showed the dependence of the growth rate and consequent up-regulation of TSST-1 encoding gene on storage time-temperature and type of milk. In contaminated pasteurized and UHT milk kept at both 15 °C and 22 °C S. aureus significantly increased its virulent potential over time. This effect was a bit more emphasized in UHT milk serving as a "proof of concept". Possible explanation could be a presence of lactic acid bacteria in pasteurized milk which is known to have down-regulatory effect on TSST-1 gene. Maintenance of the milk storage temperature below 8 °C and employment of microbiological control measures in hygienic practices, from milk producer through retailer and on to the consumer is of utmost importance to decrease risk of non-emetic staphylococcal poisoning.

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Superantigenic activity of toxic shock syndrome toxin-1 is resistant to heating and digestive enzymes

Cited by 26 publications

References 38 publications

Identification and Characterization of a Novel Staphylococcal Emetic Toxin

Identification and Characterization of a Novel Staphylococcal Emetic Toxin

Submucosal mast cells in the gastrointestinal tract are a target of staphylococcal enterotoxin type A

Expression of toxic shock syndrome toxin-1 gene of Staphylococcus aureus in milk: Proof of concept

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