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

• Published in: FEMS immunology and medical microbiology Vol. 64; no. 3; pp. 392 - 402
• Main Authors: Ono, Hisaya K., Nishizawa, Masato, Yamamoto, Yoshio, Hu, Dong-Liang, Nakane, Akio, Shinagawa, Kunihiro, Omoe, Katsuhiko
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.04.2012; Blackwell; Oxford University Press
• Subjects: Animals; Bacterial Toxins - metabolism; Bacteriology; Binding; Biological and medical sciences; Degranulation; emesis; Enterotoxins - metabolism; Food contamination; Food poisoning; Fundamental and applied biological sciences. Psychology; Gastrointestinal system; Gastrointestinal tract; Gastrointestinal Tract - metabolism; Histamine; Immunofluorescence; In vivo methods and tests; mast cell; Mast cells; Mast Cells - metabolism; Microbiology; Miscellaneous; Primates; Receptors, IgE - metabolism; Serotonin; Serotonin - metabolism; Shrews; staphylococcal enterotoxin; Staphylococcal enterotoxin A; Staphylococcal Food Poisoning - metabolism; Staphylococcus - metabolism; Suncus murinus; Superantigens - metabolism; Toluidine; Toluidine blue; Toxins; Tryptase; Tryptases - metabolism; Vomiting; Vomiting - chemically induced; Vomiting - metabolism; staphylococcal enterotoxin; mast cell; emesis; Toxin; Immunology; Enterotoxin; Bacteria; Micrococcales; Micrococcaceae; Mast cell; Digestive tract; Staphylococcus
• ISSN: 0928-8244; 1574-695X; 2049-632X
• DOI: 10.1111/j.1574-695X.2011.00924.x

Abstract 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.