Goblet cells are involved in translocation of staphylococcal enterotoxin A in the intestinal tissue of house musk shrew (<i>Suncus murinus</i>
)

Hirose, Shouhei; Ono, Hisaya K.; Omoe, Katsuhiko; Hu, Dong‐Liang; Asano, Kozo; Yamamoto, Yoshio; Nakane, Akio

doi:10.1111/jam.13029

Cited by 16 publications

(12 citation statements)

References 26 publications

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“…Bacterial toxins are considered to be one of the most common causes of foodborne disease outbreaks worldwide [1]. Staphylococcus aureus (S. aureus), a common foodborne pathogen, causes foodborne poisoning and toxic shock syndrome by secreting bacterial superantigen toxins (staphylococcal enterotoxins, SEs) [2]. Staphylococcal food poisoning (SFP) caused by the ingestion of pre-formed SE contaminated food is one of the most prevalent bacterial foodborne diseases, and can cause severe food safety, public health and economic problems [3].…”

Section: Introductionmentioning

confidence: 99%

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Liu

Chi

Yang

et al. 2022

Toxins

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Staphylococcal enterotoxin A (SEA), the toxin protein secreted by Staphylococcus aureus, can cause staphylococcal food poisoning outbreaks and seriously threaten global public health. However, little is known about the pathogenesis of SEA in staphylococcal foodborne diseases. In this study, the effect of SEA on intestinal barrier injury and NLRP3 inflammasome activation was investigated by exposing BALB/c mice to SEA with increasing doses and a potential toxic mechanism was elucidated. Our findings suggested that SEA exposure provoked villi injury and suppressed the expression of ZO-1 and occludin proteins, thereby inducing intestinal barrier dysfunction and small intestinal injury in mice. Concurrently, SEA significantly up-regulated the expression of NLRP3 inflammasome-associated proteins and triggered the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways in jejunum tissues. Notably, selective inhibitors of MAPKs and NF-κB p65 ameliorated the activation of NLRP3 inflammasome stimulated by SEA, which further indicated that SEA could activate NLRP3 inflammasome through NF-κB/MAPK pathways. In summary, SEA was first confirmed to induce intestinal barrier dysfunction and activate NLRP3 inflammasome via NF-κB/MAPK signaling pathways. These findings will contribute to a more comprehensive understanding of the pathogenesis of SEA and related drug-screening for the treatment and prevention of bacteriotoxin-caused foodborne diseases via targeting specific pathways.

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Section: Introductionmentioning

confidence: 99%

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Liu

Chi

Yang

et al. 2022

Toxins

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“…Other agonists involved in the emetic response have also been reported (Scheuber et al, 1987 ; Alber et al, 1989 ; Jett et al, 1990 ). In addition to mast cells, the SEs appear to have an affinity for epithelial cells (Hamad et al, 1997 ; Shupp et al, 2002 ; Danielsen et al, 2013 ; Zhao et al, 2016a ) and goblet cells (Hirose et al, 2016 ). Unlike mast cells, SEs use epithelial cells (Danielsen et al, 2013 ) and mucus-producing goblet cells (Hirose et al, 2016 ) as gateways in order to traffic across the intestinal epithelia to reach other final targets.…”

Section: Mechanisms Underlying Enterotoxin-induced Emetic and Diarrhementioning

confidence: 99%

“…In addition to mast cells, the SEs appear to have an affinity for epithelial cells (Hamad et al, 1997 ; Shupp et al, 2002 ; Danielsen et al, 2013 ; Zhao et al, 2016a ) and goblet cells (Hirose et al, 2016 ). Unlike mast cells, SEs use epithelial cells (Danielsen et al, 2013 ) and mucus-producing goblet cells (Hirose et al, 2016 ) as gateways in order to traffic across the intestinal epithelia to reach other final targets. Importantly, the movement of enterotoxins through epithelial cells is thought to be a glycolipid-dependent transcytosis process that may be facilitated in the presence of other S. aureus virulence determinants (Edwards et al, 2012 ).…”

Section: Mechanisms Underlying Enterotoxin-induced Emetic and Diarrhementioning

confidence: 99%

Basis of Virulence in Enterotoxin-Mediated Staphylococcal Food Poisoning

2018

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The Staphylococcus aureus enterotoxins are a superfamily of secreted virulence factors that share structural and functional similarities and possess potent superantigenic activity causing disruptions in adaptive immunity. The enterotoxins can be separated into two groups; the classical (SEA-SEE) and the newer (SEG-SElY and counting) enterotoxin groups. Many members from both these groups contribute to the pathogenesis of several serious human diseases, including toxic shock syndrome, pneumonia, and sepsis-related infections. Additionally, many members demonstrate emetic activity and are frequently responsible for food poisoning outbreaks. Due to their robust tolerance to denaturing, the enterotoxins retain activity in food contaminated previously with S. aureus. The genes encoding the enterotoxins are found mostly on a variety of different mobile genetic elements. Therefore, the presence of enterotoxins can vary widely among different S. aureus isolates. Additionally, the enterotoxins are regulated by multiple, and often overlapping, regulatory pathways, which are influenced by environmental factors. In this review, we also will focus on the newer enterotoxins (SEG-SElY), which matter for the role of S. aureus as an enteropathogen, and summarize our current knowledge on their prevalence in recent food poisoning outbreaks. Finally, we will review the current literature regarding the key elements that govern the complex regulation of enterotoxins, the molecular mechanisms underlying their enterotoxigenic, superantigenic, and immunomodulatory functions, and discuss how these activities may collectively contribute to the overall manifestation of staphylococcal food poisoning.

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“…Recent studies investigated the behavior of SEA in the gastrointestinal tract of house musk shrew and common marmoset, suggesting that submucosal mast cells in the gastrointestinal tract are one of the target cells of SEs. Histamin and serotonine (5-HT) released from submucosal mast cells play an important role in SE-induced emesis (Hirose et al 2016;Hu et al 2007;Ono et al 2012Ono et al , 2019. In addition, vagotomy prevented vomiting caused by SEA in the emetic-inducing animal model, indicating that 5-HT may bind to 5-HT 3 receptors, expressed on the enteric nerves of the gastrointestinal tract, thereby causing these nerves to deprive polarization (Hu et al 2007;Ono et al 2017Ono et al , 2019.…”

Section: Biological Characteristics and Activities Of Sag Toxinsmentioning

confidence: 99%

Update on molecular diversity and multipathogenicity of staphylococcal superantigen toxins

Fang

et al. 2021

Animal Diseases

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Staphylococcal superantigen (SAg) toxins are the most notable virulence factors associated with Staphylococcus aureus, which is a pathogen associated with serious community and hospital acquired infections in humans and various diseases in animals. Recently, SAg toxins have become a superfamily with 29 types, including staphylococcal enterotoxins (SEs) with emetic activity, SE-like toxins (SEls) that do not induce emesis in primate models or have yet not been tested, and toxic shock syndrome toxin-1 (TSST-1). SEs and SEls can be subdivided into classical types (SEA to SEE) and novel types (SEG to SElY, SE01, SE02, SEl26 and SEl27). The genes of SAg toxins are located in diverse accessory genetic elements and share certain structural and biological properties. SAg toxins are heat-stable proteins that exhibit pyrogenicity, superantigenicity and capacity to induce lethal hypersensitivity to endotoxin in humans and animals. They have multiple pathogenicities that can interfere with normal immune function of host, increase the chances of survival and transmission of pathogenic bacteria in host, consequently contribute to the occurrence and development of various infections, persistent infections or food poisoning. This review focuses on the following aspects of SAg toxins: (1) superfamily members of classic and novelty discovered staphylococcal SAgs; (2) diversity of gene locations and molecular structural characteristics; (3) biological characteristics and activities; (4) multi-pathogenicity of SAgs in animal and human diseases, including bovine mastitis, swine sepsis, abscesses and skin edema in pig, arthritis and septicemia in poultry, and nosocomial infections and food-borne diseases in humans.

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Goblet cells are involved in translocation of staphylococcal enterotoxin A in the intestinal tissue of house musk shrew (Suncus murinus )

Abstract: An entry site of SEA during translocation across the gastrointestinal mucosal barrier was investigated. This study was the first to demonstrate the significance of goblet cells as an entry site of this bacterial toxin.

Cited by 16 publications

References 26 publications

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Staphylococcal Enterotoxin A Induces Intestinal Barrier Dysfunction and Activates NLRP3 Inflammasome via NF-κB/MAPK Signaling Pathways in Mice

Basis of Virulence in Enterotoxin-Mediated Staphylococcal Food Poisoning

Update on molecular diversity and multipathogenicity of staphylococcal superantigen toxins

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