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Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses

Staphylococcal enterotoxin B (SEB) and related exotoxins are important virulence factors produced by Staphylococcus aureus as they cause human diseases such as food poisoning and toxic shock. These toxins bind directly to cells of the immune system resulting in hyperactivation of both T lymphocytes...

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Detalles Bibliográficos
Autor principal: Krakauer, Teresa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4344640/
https://www.ncbi.nlm.nih.gov/pubmed/25688664
http://dx.doi.org/10.3390/toxins7020553
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author Krakauer, Teresa
author_facet Krakauer, Teresa
author_sort Krakauer, Teresa
collection PubMed
description Staphylococcal enterotoxin B (SEB) and related exotoxins are important virulence factors produced by Staphylococcus aureus as they cause human diseases such as food poisoning and toxic shock. These toxins bind directly to cells of the immune system resulting in hyperactivation of both T lymphocytes and monocytes/macrophages. The excessive release of proinflammatory cytokines from these cells mediates the toxic effects of SEB. This study examined the inhibitory activities of an anti-inflammatory drug, sulfasalazine, on SEB-stimulated human peripheral blood mononuclear cells (PBMC). Sulfasalazine dose-dependently inhibited tumor necrosis factor α, interleukin 1 (IL-1) β, IL-2, IL-6, interferon γ (IFNγ), and various chemotactic cytokines from SEB-stimulated human PBMC. Sulfasalazine also potently blocked SEB-induced T cell proliferation and NFκB activation. These results suggest that sulfasalazine might be useful in mitigating the toxic effects of SEB by blocking SEB-induced host inflammatory cascade and signaling pathways.
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spelling pubmed-43446402015-03-18 Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses Krakauer, Teresa Toxins (Basel) Article Staphylococcal enterotoxin B (SEB) and related exotoxins are important virulence factors produced by Staphylococcus aureus as they cause human diseases such as food poisoning and toxic shock. These toxins bind directly to cells of the immune system resulting in hyperactivation of both T lymphocytes and monocytes/macrophages. The excessive release of proinflammatory cytokines from these cells mediates the toxic effects of SEB. This study examined the inhibitory activities of an anti-inflammatory drug, sulfasalazine, on SEB-stimulated human peripheral blood mononuclear cells (PBMC). Sulfasalazine dose-dependently inhibited tumor necrosis factor α, interleukin 1 (IL-1) β, IL-2, IL-6, interferon γ (IFNγ), and various chemotactic cytokines from SEB-stimulated human PBMC. Sulfasalazine also potently blocked SEB-induced T cell proliferation and NFκB activation. These results suggest that sulfasalazine might be useful in mitigating the toxic effects of SEB by blocking SEB-induced host inflammatory cascade and signaling pathways. MDPI 2015-02-13 /pmc/articles/PMC4344640/ /pubmed/25688664 http://dx.doi.org/10.3390/toxins7020553 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Krakauer, Teresa
Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses
title Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses
title_full Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses
title_fullStr Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses
title_full_unstemmed Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses
title_short Sulfasalazine Attenuates Staphylococcal Enterotoxin B-Induced Immune Responses
title_sort sulfasalazine attenuates staphylococcal enterotoxin b-induced immune responses
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4344640/
https://www.ncbi.nlm.nih.gov/pubmed/25688664
http://dx.doi.org/10.3390/toxins7020553
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