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Diesner, S.C.* ; Bergmayr, C.* ; Pfitzner, B. ; Assmann, V.E.* ; Krishnamurthy, D.* ; Starkl, P.* ; Endesfelder, D. ; Rothballer, M. ; Welzl, G. ; Rattei, T.* ; Eiwegger, T.* ; Szepfalusi, Z.* ; Fehrenbach, H.* ; Jensen-Jarolim, E.* ; Hartmann, A. ; Pali-Scholl, I.* ; Untersmayr, E.*

A distinct microbiota composition is associated with protection from food allergy in an oral mouse immunization model.

Clin. Immunol. 173, 10-18 (2016)
Verlagsversion DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
In our mouse model, gastric acid-suppression is associated with antigen-specific IgE and anaphylaxis development. We repeatedly observed non-responder animals protected from food allergy. Here, we aimed to analyse reasons for this protection. Ten out of 64 mice, subjected to oral ovalbumin (OVA) immunizations under gastric acid-suppression, were non-responders without OVA-specific IgE or IgG1 elevation, indicating protection from allergy. In these non-responders, allergen challenges confirmed reduced antigen uptake and lack of anaphylactic symptoms, while in allergic mice high levels of mouse mast-cell protease-1 and a body temperature reduction, indicative for anaphylaxis, were determined. Upon OVA stimulation, significantly lower IL-4, IL-5, IL-10 and IL-13 levels were detected in non-responders, while IL-22 was significantly higher. Comparison of fecal microbiota revealed differences of bacterial communities on single bacterial Operational-Taxonomic-Unit level between the groups, indicating protection from food allergy being associated with a distinct microbiota composition in a non-responding phenotype in this mouse model.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Allergen Uptake ; Bacterial Community Composition ; Cytokines ; Food Allergy ; Intestinal Barrier Function ; Microbiota; Balb/c Mice; Antacid Medication; Immunoglobulin-a; Acid-suppression; Murine Models; Sensitization; Gut; Anaphylaxis; Bacteria; Disease
ISSN (print) / ISBN 1521-6616
e-ISSN 1521-7035
Zeitschrift Clinical Immunology
Quellenangaben Band: 173, Heft: , Seiten: 10-18 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort San Diego
Begutachtungsstatus Peer reviewed