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Mouse strain-dependent difference toward the staphylococcus aureus allergen serine protease-like protein D reveals a novel regulator of IL-33

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Abstract
Staphylococcus aureus (S. aureus) can secrete a broad range of virulence factors, among which staphylococcal serine protease-like proteins (Spls) have been identified as bacterial allergens. The S. aureus allergen serine protease-like protein D (SplD) induces allergic asthma in C57BL/6J mice through the IL-33/ST2 signaling axis. Analysis of C57BL/6J, C57BL/6N, CBA, DBA/2, and BALB/c mice treated with intratracheal applications of SplD allowed us to identify a frameshift mutation in the serine (or cysteine) peptidase inhibitor, clade A, and member 3I (Serpina3i) causing a truncated form of SERPINA3I in BALB/c, CBA, and DBA/2 mice. IL-33 is a key mediator of SplD-induced immunity and can be processed by proteases leading to its activation or degradation. Full-length SERPINA3I inhibits IL-33 degradation in vivo in the lungs of SplD-treated BALB/c mice and in vitro by direct inhibition of mMCP-4. Collectively, our results establish SERPINA3I as a regulator of IL-33 in the lungs following exposure to the bacterial allergen SplD, and that the asthma phenotypes of mouse strains may be strongly influenced by the observed frameshift mutation in Serpina3i. The analysis of this protease-serpin interaction network might help to identify predictive biomarkers for type-2 biased airway disease in individuals colonized by S. aureus.
Keywords
allergy, asthma, IL-33, S, aureus, SplD, type 2 immunity, MAST-CELL CHYMASE, ASTHMA, INTERLEUKIN-33, RESPONSES, CLEAVAGE, ANTICHYMOTRYPSIN, ASSOCIATION, ACTIVATION, EXPRESSION, CYTOKINE

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MLA
Teufelberger, Andrea Renate, et al. “Mouse Strain-Dependent Difference toward the Staphylococcus Aureus Allergen Serine Protease-like Protein D Reveals a Novel Regulator of IL-33.” FRONTIERS IN IMMUNOLOGY, vol. 11, 2020, doi:10.3389/fimmu.2020.582044.
APA
Teufelberger, A. R., Van Nevel, S., Hulpiau, P., Nordengrün, M., Savvides, S., De Graeve, S., … Krysko, O. (2020). Mouse strain-dependent difference toward the staphylococcus aureus allergen serine protease-like protein D reveals a novel regulator of IL-33. FRONTIERS IN IMMUNOLOGY, 11. https://doi.org/10.3389/fimmu.2020.582044
Chicago author-date
Teufelberger, Andrea Renate, Sharon Van Nevel, Paco Hulpiau, Maria Nordengrün, Savvas Savvides, Sarah De Graeve, Srinivas Akula, et al. 2020. “Mouse Strain-Dependent Difference toward the Staphylococcus Aureus Allergen Serine Protease-like Protein D Reveals a Novel Regulator of IL-33.” FRONTIERS IN IMMUNOLOGY 11. https://doi.org/10.3389/fimmu.2020.582044.
Chicago author-date (all authors)
Teufelberger, Andrea Renate, Sharon Van Nevel, Paco Hulpiau, Maria Nordengrün, Savvas Savvides, Sarah De Graeve, Srinivas Akula, Gabriële Holtappels, Natalie De Ruyck, Wim Declercq, Peter Vandenabeele, Lars Hellman, Barbara M. Bröker, Dmitri Krysko, Claus Bachert, and Olga Krysko. 2020. “Mouse Strain-Dependent Difference toward the Staphylococcus Aureus Allergen Serine Protease-like Protein D Reveals a Novel Regulator of IL-33.” FRONTIERS IN IMMUNOLOGY 11. doi:10.3389/fimmu.2020.582044.
Vancouver
1.
Teufelberger AR, Van Nevel S, Hulpiau P, Nordengrün M, Savvides S, De Graeve S, et al. Mouse strain-dependent difference toward the staphylococcus aureus allergen serine protease-like protein D reveals a novel regulator of IL-33. FRONTIERS IN IMMUNOLOGY. 2020;11.
IEEE
[1]
A. R. Teufelberger et al., “Mouse strain-dependent difference toward the staphylococcus aureus allergen serine protease-like protein D reveals a novel regulator of IL-33,” FRONTIERS IN IMMUNOLOGY, vol. 11, 2020.
@article{8676737,
  abstract     = {{Staphylococcus aureus (S. aureus) can secrete a broad range of virulence factors, among which staphylococcal serine protease-like proteins (Spls) have been identified as bacterial allergens. The S. aureus allergen serine protease-like protein D (SplD) induces allergic asthma in C57BL/6J mice through the IL-33/ST2 signaling axis. Analysis of C57BL/6J, C57BL/6N, CBA, DBA/2, and BALB/c mice treated with intratracheal applications of SplD allowed us to identify a frameshift mutation in the serine (or cysteine) peptidase inhibitor, clade A, and member 3I (Serpina3i) causing a truncated form of SERPINA3I in BALB/c, CBA, and DBA/2 mice. IL-33 is a key mediator of SplD-induced immunity and can be processed by proteases leading to its activation or degradation. Full-length SERPINA3I inhibits IL-33 degradation in vivo in the lungs of SplD-treated BALB/c mice and in vitro by direct inhibition of mMCP-4. Collectively, our results establish SERPINA3I as a regulator of IL-33 in the lungs following exposure to the bacterial allergen SplD, and that the asthma phenotypes of mouse strains may be strongly influenced by the observed frameshift mutation in Serpina3i. The analysis of this protease-serpin interaction network might help to identify predictive biomarkers for type-2 biased airway disease in individuals colonized by S. aureus.}},
  articleno    = {{582044}},
  author       = {{Teufelberger, Andrea Renate and Van Nevel, Sharon and Hulpiau, Paco and Nordengrün, Maria and Savvides, Savvas and De Graeve, Sarah and Akula, Srinivas and Holtappels, Gabriële and De Ruyck, Natalie and Declercq, Wim and Vandenabeele, Peter and Hellman, Lars and Bröker, Barbara M. and Krysko, Dmitri and Bachert, Claus and Krysko, Olga}},
  issn         = {{1664-3224}},
  journal      = {{FRONTIERS IN IMMUNOLOGY}},
  keywords     = {{allergy,asthma,IL-33,S,aureus,SplD,type 2 immunity,MAST-CELL CHYMASE,ASTHMA,INTERLEUKIN-33,RESPONSES,CLEAVAGE,ANTICHYMOTRYPSIN,ASSOCIATION,ACTIVATION,EXPRESSION,CYTOKINE}},
  language     = {{eng}},
  pages        = {{13}},
  title        = {{Mouse strain-dependent difference toward the staphylococcus aureus allergen serine protease-like protein D reveals a novel regulator of IL-33}},
  url          = {{http://dx.doi.org/10.3389/fimmu.2020.582044}},
  volume       = {{11}},
  year         = {{2020}},
}

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