Abstract
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.
Highlights
Introduction iationsBacterial toxins are considered to be one of the most common causes of foodborne disease outbreaks worldwide [1]
Key Contribution: Our study demonstrated for the first time that Staphylococcal enterotoxin A (SEA) exposure could cause villi injury and inhibit the expression of tight junction (TJ) proteins, thereby inducing intestinal barrier dysfunction and small intestinal injury
These results indicated that the sea gene was successfully inserted into the pET-28a vector
Summary
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]. The corresponding symptoms mainly include nausea, vomiting, abdominal cramping and diarrhea. SEs are widely distributed in food processing environments, workers’ skin, food production animals, and frequently contaminate raw milk and dairy products, raw meat and meat products, ready-to-eat food, etc. SEs toxin protein is highly resistant to harsh-sterilization environments during SEs are widely distributed in food processing environments, workers’ skin, food production animals, and frequently contaminate raw milk and dairy products, raw meat and meat products, ready-to-eat food, etc. [4,5].
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