Abstract | BACKGROUND: METHODS: Wild-type (WT) and IL-17RE deficient (Il-17re-/-) mice were sensitized and challenged with OVA to induce allergic airway inflammation. pIC or PBS were applied intranasally when allergic airway inflammation had been established. Pulmonary expression of inflammatory mediators, numbers of inflammatory cells, and airway hyperresponsiveness (AHR) were analyzed. RESULTS: Ablation of IL-17RE did not affect the development of OVA-induced allergic airway inflammation and AHR. pIC induced inflammation independent of IL-17RE in the absence of allergic airway inflammation. Treatment of mice with pIC exacerbated pulmonary inflammation in sensitized and OVA-challenged mice in an IL-17RE-dependent manner. The pIC-induced expression of cytokines (e.g. keratinocyte-derived chemokine (KC), granulocyte-colony stimulating factor ( G-CSF)) and recruitment of neutrophils were decreased in Il-17re-/- mice. pIC-exacerbated AHR was partially decreased in Il-17re-/- mice. CONCLUSIONS: Our results indicate that IL-17RE mediates virus-triggered exacerbations but does not have a function in the development of allergic lung disease.
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Authors | Giovanna Vella, Lars Lunding, Felix Ritzmann, Anja Honecker, Christian Herr, Michael Wegmann, Robert Bals, Christoph Beisswenger |
Journal | Respiratory research
(Respir Res)
Vol. 21
Issue 1
Pg. 176
(Jul 08 2020)
ISSN: 1465-993X [Electronic] England |
PMID | 32641167
(Publication Type: Journal Article)
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Chemical References |
- Cytokines
- IL17A protein, human
- Il17ra protein, mouse
- Inflammation Mediators
- Interleukin-17
- Receptors, Interleukin-17
- Ovalbumin
- Poly I-C
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Topics |
- Animals
- Asthma
(chemically induced, physiopathology)
- Bronchoalveolar Lavage Fluid
(cytology)
- Cytokines
(biosynthesis)
- Epithelial Cells
- Inflammation Mediators
(metabolism)
- Interleukin-17
- Lung
(pathology)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Neutrophil Infiltration
- Ovalbumin
(immunology)
- Poly I-C
- Receptors, Interleukin-17
(genetics, metabolism)
- Respiratory Hypersensitivity
(metabolism)
- Respiratory Mucosa
(cytology, metabolism)
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