Publikationsdatenbank

Intranasal Staphylococcus aureus enterotoxin B modulates allergic airway inflammation in a dose- and time-dependent manner in a mouse model (2021)

Art

Vortrag

Autoren

Stegemann-Koniszewski, S.

Jorde, I.

Hildebrand, C.

Kershaw, O. (WE 12)

Lucke, E.

Schreiber, J.

Kongress

33. Mainzer Allergie-Workshop, Frühjahrstagung der DGAKI

Mainz, 25. – 26.03.2021

Quelle

Allergologie : immunbiologische Grundlagen ; Diagnostik und Therapie für Praxis und Klinik ; Organ der Deutschen Gesellschaft für Allergie- und Immunitätsforschung und des Ärzteverbandes Deutscher Allergologen

Bandzählung: 44

Heftzählung: 2

Seiten: 162

ISSN: 0344-5062

Sprache

Englisch

Verweise

URL (Volltext): https://www.dustri.com/nc/de/deutschsprachige-zeitschriften/mag/allergologie/vol/jahrgang-44-2021/issue/februar-52.html

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Staphylococcus aureus ( S. aureus ) enterotoxin B (SEB) acts as a superantigen and has been proposed a central player in the associations between S. aureus nasal colonization and the development of allergic asthma. Previous experimental studies have shown SEB to aggravate allergic sensitization and allergic airway inflammation (AAI), but the underlying mechanisms are elusive to date. In our study, we hypothesized that modulation of AAI by intranasal treatment with SEB depends on the timing and the dose of SEB administration. In an ovalbuminmediated mouse model of AAI, we treated wild-type mice intranasally with 50 ng or 500 ng SEB either together with the airway allergic challenge or prior to the peripheral sensitization. SEB administration affected hallmark parameters of AAI, and the observed effects depended on the timing and the dose of treatment. When SEB was administered together with the allergic challenge, it significantly modulated respiratory leukocyte accumulation and intensified lymphocyte activation in the lung. At the higher dose, SEB induced a strong respiratory type-1 and pro-inflammatory cytokine response in AAI and alleviated airway hyperreactivity. Interestingly, intranasal administration of the lower dose of SEB prior to the peripheral allergic sensitization significantly boosted the specific IgE response detected upon challenge. Administration of the higher dose before sensitization led to a significantly reduced recruitment of leukocytes, including eosinophils, to the respiratory tract and to a significantly dampened Th-2 cytokine response, however without at the same time inducing a Th-1 or proinflammatory response. Taken together, we demonstrate a remarkably versatile potential for intranasally administered SEB to either aggravate or alleviate different hallmark parameters of allergic sensitization and AAI. Thereby our study highlights the complexity of the associations between S. aureus and allergic asthma and underlines the potential role of SEB in these associations.