Skin reactivity of unsensitized monkeys upon challenge with staphylococcal enterotoxin B: a new approach for investigating the site of toxin action

Scheuber, Peter H.; Golecki, Jochen R.; Kickhöfen, B.; Scheel, David; Beck, Georg; Hammer, D. K.

doi:10.1128/iai.50.3.869-876.1985

Cited by 56 publications

(18 citation statements)

References 18 publications

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“…The morphology of the SEA-binding cells in the submucosa at 30-90 min after SEA administration did not correspond to the morphology of myenteric nerves. Therefore, we suspected that the target cells of SEA were the mast cells because SEB elucidates degranulation of cutaneous mast cells in monkeys (Scheuber et al, 1985), and SEB also binds and induces 5-HT release from cultured rodent mast cells (Komisar et al, 1992). For determining whether SEA binds to mast cells in the (9400).…”

Section: Sea Accumulates In Submucosal Mast Cells In the Gi Tractmentioning

confidence: 99%

“…A number of cell types in the GI tract contain 5-HT, including enterochromaffin (EC) cells, neuronal cells, and mast cells. Especially, it has been reported that intradermally injection of SEB caused immediate-type skin reaction through degranulation of cutaneous mast cells in cynomolgus monkeys (Scheuber et al, 1985). Also, SEB induced release of 5-HT from murine mast cells in vitro (Komisar et al, 1992).…”

Section: Introductionmentioning

confidence: 98%

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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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Section: Sea Accumulates In Submucosal Mast Cells In the Gi Tractmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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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“…Mast cells could also participate in the first step of the immune response, since it was elegantly demonstrated that rodent mast cells express major histocompatibility complex (MHC) class II molecules [29][30][31][32][33][34] and have the capacity to process nominal antigens and present immunogenic peptides to T cells [31,35,36]. The possible involvement of signaling via MHC class II molecules in specific immunological processes is further reinforced by the observation that, in some primates, connective tissue mast cells were detected undergoing degranulation after intradermal injection of staphylococcal enterotoxin B (SEB) [37][38][39], a natural ligand of MHC class II molecules that does not require processing by antigen-presenting cells in order to activate T cells [40].…”

Section: Introductionmentioning

confidence: 99%

Expression of functional major histocompatility complex class II molecules on HMC-1 human mast cells

Dimitriadou

Mécheri

Koutsilieris

et al. 1998

Journal of Leukocyte Biology

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“…On the other hand, other cell types may also be involved. Scheuber and coworkers (37,38) have shown that SEB injected intradermally into cynomolgus monkeys results in an immediate-type skin hypersensitivity reaction which is caused mostly by degranulation of mast cells. This mast cell degranulation may be caused by a direct activation by SEB of mast cells or of nerve cells which release neuropeptides, which then activate mast cells (1).…”

mentioning

confidence: 99%

Immunity and responses of circulating leukocytes and lymphocytes in monkeys to aerosolized staphylococcal enterotoxin B

et al. 1993

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Rhesus monkeys immunized intramuscularly or orally with staphylococcal enterotoxin B (SEB) toxoid or SEB toxoid incorporated in microspheres made of poly(DL-lactide-co-glycolide) were challenged with a lethal dose of aerosolized SEB to study their immunity and cellular responses in the circulation. It was found that circulating antibodies play a critical role in preventing SEB from triggering toxicosis. Monkeys with high levels of antibodies survived, while those with low levels underwent 2 to 3 days of toxicosis and died. Intramuscular immunization induced high levels and oral immunization induced low levels of antibodies. The circulating antibodies in surviving monkeys decreased dramatically within 20 min and started to rebound at 90 min after SEB challenge. At 90 min, the dying monkeys showed in the circulation a dramatic increase of polymorphonuclear leukocytes and decreases of NK cells and monocytes (CD16 and CD56 markers) as well as of lymphocytes with HLA-DR, CD2, CD8, and IL2Ra (CD25) markers. The number of polymorphonuclear leukocytes showed an inverse correlation with the numbers of monocytes and various lymphocyte subpopulations which, except for IL-2R, CD16, and CD56(+) cells, showed a direct correlation with one another. The changes in the populations of leukocytes, monocytes, NK cells, and lymphocytes seem to be an indication of initial toxicosis; however, the roles of these cells in toxicosis and death remain to be defined.Staphylococcal enterotoxin B (SEB) causes food poisoning when ingested and toxic shock when it enters the blood circulation and affects systemic tissues (3,6,10,16,19,39,44). The pathological mechanisms of toxicosis and death are still largely unknown. SEB, a superantigen, binds to class II histocompatibility antigens on antigen-presenting cells, and the SEB-class II antigen complex is then presented to and activates T cells bearing certain T-cell antigen receptor V,B elements (11,22). It has been suggested that activation of both the antigen-presenting cells and T cells results in the production of large amounts of monokines and lymphokines, which cause the disease (21,26). On the other hand, other cell types may also be involved. Scheuber and coworkers (37, 38) have shown that SEB injected intradermally into cynomolgus monkeys results in an immediate-type skin hypersensitivity reaction which is caused mostly by degranulation of mast cells. This mast cell degranulation may be caused by a direct activation by SEB of mast cells or of nerve cells which release neuropeptides, which then activate mast cells (1). Histamine H2 receptor antagonists can block SEB-induced emesis and skin reactions (37). Recently, we have also shown that SEB can induce serotonin release from cultured mast cells (23).If SEB intoxication is caused by activated macrophages, T cells, and other cell types and their mediators, the toxicosis could be a cascade and/or a combination of sequential pathophysiological changes among functionally interrelated tissues. A blockade of the initial phase in which SEB reacts ...

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Skin reactivity of unsensitized monkeys upon challenge with staphylococcal enterotoxin B: a new approach for investigating the site of toxin action

Cited by 56 publications

References 18 publications

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

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

Expression of functional major histocompatility complex class II molecules on HMC-1 human mast cells

Immunity and responses of circulating leukocytes and lymphocytes in monkeys to aerosolized staphylococcal enterotoxin B

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