Average rating
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Star rating
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Authors
Joean, OanaHueber, Anja
Feller, Felix
Jirmo, Adan Chari
Lochner, Matthias
Dittrich, Anna-Maria
Albrecht, Melanie
Issue Date
2017-11-10
Metadata
Show full item recordAbstract
Because Th17-polarized airway inflammation correlates with poor control in bronchial asthma and is a feature of numerous other difficult-to-treat inflammatory lung diseases, new therapeutic approaches for this type of airway inflammation are necessary. We assessed different licensed anti-inflammatory agents with known or expected efficacy against Th17-polarization in mouse models of Th17-dependent airway inflammation. Upon intravenous transfer of in vitro derived Th17 cells and intranasal challenge with the corresponding antigen, we established acute and chronic murine models of Th17-polarised airway inflammation. Consecutively, we assessed the efficacy of methylprednisolone, roflumilast, azithromycin, AM80 and rapamycin against acute or chronic Th17-dependent airway inflammation. Quantifiers for Th17-associated inflammation comprised: bronchoalveolar lavage (BAL) differential cell counts, allergen-specific cytokine and immunoglobulin secretion, as well as flow cytometric phenotyping of pulmonary inflammatory cells. Only rapamycin proved effective against acute Th17-dependent airway inflammation, accompanied by increased plasmacytoid dendritic cells (pDCs) and reduced neutrophils as well as reduced CXCL-1 levels in BAL. Chronic Th17-dependent airway inflammation was unaltered by rapamycin treatment. None of the other agents showed efficacy in our models. Our results demonstrate that Th17-dependent airway inflammation is difficult to treat with known agents. However, we identify rapamycin as an agent with inhibitory potential against acute Th17-polarized airway inflammation.Citation
Suppression of Th17-polarized airway inflammation by rapamycin. 2017, 7 (1):15336 Sci RepAffiliation
TWINCORE, Zentrum für experimentelle und kliische Infektionsforschung GmbH, Deodor-Lynen-Sr. 7, 30625 Hannover, Germany.Journal
Scientific reportsPubMed ID
29127369Type
ArticleLanguage
enISSN
2045-2322ae974a485f413a2113503eed53cd6c53
10.1038/s41598-017-15750-6
Scopus Count
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
Related articles
- Bu-Shen-Yi-Qi formulae suppress chronic airway inflammation and regulate Th17/Treg imbalance in the murine ovalbumin asthma model.
- Authors: Wei Y, Luo QL, Sun J, Chen MX, Liu F, Dong JC
- Issue date: 2015 Apr 22
- Critical role of IL-6 in dendritic cell-induced allergic inflammation of asthma.
- Authors: Lin YL, Chen SH, Wang JY
- Issue date: 2016 Jan
- Epigallocatechin gallate improves airway inflammation through TGF‑β1 signaling pathway in asthmatic mice.
- Authors: Shan L, Kang X, Liu F, Cai X, Han X, Shang Y
- Issue date: 2018 Aug
- Curcumin attenuates allergic airway inflammation by regulation of CD4+CD25+ regulatory T cells (Tregs)/Th17 balance in ovalbumin-sensitized mice.
- Authors: Ma C, Ma Z, Fu Q, Ma S
- Issue date: 2013 Jun
- Selective down-regulation of Th2 cell-mediated airway inflammation in mice by pharmacological intervention of CCR4.
- Authors: Kaminuma O, Ohtomo T, Mori A, Nagakubo D, Hieshima K, Ohmachi Y, Noda Y, Katayama K, Suzuki K, Motoi Y, Kitamura N, Saeki M, Nishimura T, Yoshie O, Hiroi T
- Issue date: 2012 Feb