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The adjuvant-like activity of staphylococcal enterotoxin B in a murine asthma model is independent of IL-1R signaling

Olga Krysko (UGent) , Tania Maes (UGent) , Maud Plantinga (UGent) , Gabriële Holtappels (UGent) , Rosina Imiru (UGent) , Peter Vandenabeele (UGent) , Guy Joos (UGent) , Dmitri Krysko (UGent) and Claus Bachert (UGent)
(2013) ALLERGY. 68(4). p.446-453
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Abstract
Background: Staphylococcal enterotoxin B (SEB) is a superantigen known to be a modulator of chronic airway inflammation in mice and humans, yet little is known about the mechanisms that regulate its interaction with the innate immune system. We investigated this mechanism in a murine model of allergic airway inflammation induced by OVA (ovalbumin) in the presence of SEB. Methods: Superantigen-induced allergic inflammation was studied in IL-1R knockout (KO) mice exposed to OVA+SEB. Multicolor flow cytometry was used to analyze the inflammatory cell profile in airways and lymph nodes. Production of IL-4, IL-5, IL-10, and IL-13 in lymph nodes was assessed by Luminex technology. Results: In wild-type mice, endonasal instillation of OVA+SEB induced a pulmonary inflammation, characterized by an increase in the number of eosinophils, T cells, and dendritic cells and in the production of Th2 cytokines and OVA-specific IgE. In IL-1R KO mice exposed to OVA+SEB, attraction of CD4+ cells and production of Th2 cytokines were reduced. However, knocking out IL-1R did not affect any of the features of allergic airway inflammation, such as bronchial eosinophilia, OVA-specific IgE production and goblet cell metaplasia. Conclusion: We provide new insights into the mechanisms of airways allergy development in the presence of bacterial superantigen. The asthma features induced by OVA+SEB, such as bronchial eosinophilia, goblet cell proliferation, production of OVA-specific IgE and increase in inflammatory dendritic cells, are IL-1R independent. Yet, IL-1R signaling is crucial for CD4 cell accumulation and Th2 cytokine production.
Keywords
staphylococcal enterotoxin B, asthma, superantigen, T cells, IMMUNE-RESPONSES, CELL-ACTIVATION, HYPERSENSITIVITY RESPONSE, ALUMINUM ADJUVANT, ATOPIC-DERMATITIS, TH2 RESPONSES, NASAL POLYPS, AUREUS, MICE, INFLAMMATION

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MLA
Krysko, Olga, Tania Maes, Maud Plantinga, et al. “The Adjuvant-like Activity of Staphylococcal Enterotoxin B in a Murine Asthma Model Is Independent of IL-1R Signaling.” ALLERGY 68.4 (2013): 446–453. Print.
APA
Krysko, O., Maes, T., Plantinga, M., Holtappels, G., Imiru, R., Vandenabeele, P., Joos, G., et al. (2013). The adjuvant-like activity of staphylococcal enterotoxin B in a murine asthma model is independent of IL-1R signaling. ALLERGY, 68(4), 446–453.
Chicago author-date
Krysko, Olga, Tania Maes, Maud Plantinga, Gabriële Holtappels, Rosina Imiru, Peter Vandenabeele, Guy Joos, Dmitri Krysko, and Claus Bachert. 2013. “The Adjuvant-like Activity of Staphylococcal Enterotoxin B in a Murine Asthma Model Is Independent of IL-1R Signaling.” Allergy 68 (4): 446–453.
Chicago author-date (all authors)
Krysko, Olga, Tania Maes, Maud Plantinga, Gabriële Holtappels, Rosina Imiru, Peter Vandenabeele, Guy Joos, Dmitri Krysko, and Claus Bachert. 2013. “The Adjuvant-like Activity of Staphylococcal Enterotoxin B in a Murine Asthma Model Is Independent of IL-1R Signaling.” Allergy 68 (4): 446–453.
Vancouver
1.
Krysko O, Maes T, Plantinga M, Holtappels G, Imiru R, Vandenabeele P, et al. The adjuvant-like activity of staphylococcal enterotoxin B in a murine asthma model is independent of IL-1R signaling. ALLERGY. 2013;68(4):446–53.
IEEE
[1]
O. Krysko et al., “The adjuvant-like activity of staphylococcal enterotoxin B in a murine asthma model is independent of IL-1R signaling,” ALLERGY, vol. 68, no. 4, pp. 446–453, 2013.
@article{3171142,
  abstract     = {Background: Staphylococcal enterotoxin B (SEB) is a superantigen known to be a modulator of chronic airway inflammation in mice and humans, yet little is known about the mechanisms that regulate its interaction with the innate immune system. We investigated this mechanism in a murine model of allergic airway inflammation induced by OVA (ovalbumin) in the presence of SEB.
Methods: Superantigen-induced allergic inflammation was studied in IL-1R knockout (KO) mice exposed to OVA+SEB. Multicolor flow cytometry was used to analyze the inflammatory cell profile in airways and lymph nodes. Production of IL-4, IL-5, IL-10, and IL-13 in lymph nodes was assessed by Luminex technology.
Results: In wild-type mice, endonasal instillation of OVA+SEB induced a pulmonary inflammation, characterized by an increase in the number of eosinophils, T cells, and dendritic cells and in the production of Th2 cytokines and OVA-specific IgE. In IL-1R KO mice exposed to OVA+SEB, attraction of CD4+ cells and production of Th2 cytokines were reduced. However, knocking out IL-1R did not affect any of the features of allergic airway inflammation, such as bronchial eosinophilia, OVA-specific IgE production and goblet cell metaplasia.
Conclusion: We provide new insights into the mechanisms of airways allergy development in the presence of bacterial superantigen. The asthma features induced by OVA+SEB, such as bronchial eosinophilia, goblet cell proliferation, production of OVA-specific IgE and increase in inflammatory dendritic cells, are IL-1R independent. Yet, IL-1R signaling is crucial for CD4 cell accumulation and Th2 cytokine production.},
  author       = {Krysko, Olga and Maes, Tania and Plantinga, Maud and Holtappels, Gabriële and Imiru, Rosina and Vandenabeele, Peter and Joos, Guy and Krysko, Dmitri and Bachert, Claus},
  issn         = {0105-4538},
  journal      = {ALLERGY},
  keywords     = {staphylococcal enterotoxin B,asthma,superantigen,T cells,IMMUNE-RESPONSES,CELL-ACTIVATION,HYPERSENSITIVITY RESPONSE,ALUMINUM ADJUVANT,ATOPIC-DERMATITIS,TH2 RESPONSES,NASAL POLYPS,AUREUS,MICE,INFLAMMATION},
  language     = {eng},
  number       = {4},
  pages        = {446--453},
  title        = {The adjuvant-like activity of staphylococcal enterotoxin B in a murine asthma model is independent of IL-1R signaling},
  url          = {http://dx.doi.org/10.1111/all.12102},
  volume       = {68},
  year         = {2013},
}

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