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Gewählte Publikation:

Publikationstyp: Zeitschriftenaufsatz
Dokumenttyp: Originalarbeit

Jahr: 2014

AutorInnen: Rauch, I; Hainzl, E; Rosebrock, F; Heider, S; Schwab, C; Berry, D; Stoiber, D; Wagner, M; Schleper, C; Loy, A; Urich, T; Müller, M; Strobl, B; Kenner, L; Decker, T

Titel: Type I interferons have opposing effects during the emergence and recovery phases of colitis.

Quelle: Eur J Immunol. 2014; 44(9):2749-2760



Autor/innen der Vetmeduni Vienna:

Hainzl Eva
Kenner Lukas
Müller Mathias
Strobl Birgit

Beteiligte Vetmed-Organisationseinheiten
Institut für Tierzucht und Genetik, Abteilung für Molekulare Genetik


Abstract:
The contribution of the innate immune system to inflammatory bowel disease (IBD) is under intensive investigation. Research in animal models has demonstrated that type I interferons (IFN-Is) protect from IBD. In contrast, studies of patients with IBD have produced conflicting results concerning the therapeutic potential of IFN-Is. Here, we present data suggesting that IFN-Is play dual roles as regulators of intestinal inflammation in dextran sodium sulfate (DSS)-treated C57BL/6 mice. Though IFN-Is reduced acute intestinal damage and the abundance of colitis-associated intestinal bacteria caused by treatment with a high dose of DSS, they also inhibited the resolution of inflammation after DSS treatment. IFN-Is played an anti-inflammatory role by suppressing the release of IL-1β from the colon MHC class II(+) cells. Consistently, IL-1 receptor blockade reduced the severity of inflammation in IFN-I receptor-deficient mice and myeloid cell-restricted ablation of the IFN-I receptor was detrimental. The proinflammatory role of IFN-Is during recovery from DSS treatment was caused by IFN-I-dependent cell apoptosis as well as an increase in chemokine production and infiltrating inflammatory monocytes and neutrophils. Thus, IFN-Is play opposing roles in specific phases of intestinal injury and inflammation, which may be important for guiding treatment strategies in patients.

Keywords Pubmed: Animals
Colitis/chemically induced
Colitis/genetics
Colitis/immunology*
Colitis/pathology
Dextran Sulfate/toxicity
Histocompatibility Antigens Class II/genetics
Histocompatibility Antigens Class II/immunology
Inflammation/chemically induced
Inflammation/genetics
Inflammation/immunology
Inflammation/pathology
Inflammatory Bowel Diseases/chemically induced
Inflammatory Bowel Diseases/genetics
Inflammatory Bowel Diseases/immunology*
Inflammatory Bowel Diseases/pathology
Interferon Type I/genetics
Interferon Type I/immunology*
Interleukin-1beta/genetics
Interleukin-1beta/immunology
Intestines/immunology*
Intestines/pathology
Macrophages/immunology
Macrophages/pathology
Mice
Mice, Knockout
Neutrophil Infiltration/drug effects
Neutrophil Infiltration/genetics
Neutrophil Infiltration/immunology
Neutrophils/immunology
Neutrophils/pathology


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