التفاصيل البيبلوغرافية
| العنوان: |
Interleukin-33 Receptor (ST2) Deficiency Improves the Outcome of Staphylococcus aureus-Induced Septic Arthritis |
| المؤلفون: |
Larissa Staurengo-Ferrari, Silvia C. Trevelin, Victor Fattori, Daniele C. Nascimento, Kalil A. de Lima, Jacinta S. Pelayo, Florêncio Figueiredo, Rubia Casagrande, Sandra Y. Fukada, Mauro M. Teixeira, Thiago M. Cunha, Foo Y. Liew, Rene D. Oliveira, Paulo Louzada-Junior, Fernando Q. Cunha, José C. Alves-Filho, Waldiceu A. Verri |
| المصدر: |
Frontiers in Immunology, Vol 9 (2018) |
| بيانات النشر: |
Frontiers Media S.A., 2018. |
| سنة النشر: |
2018 |
| المجموعة: |
LCC:Immunologic diseases. Allergy |
| مصطلحات موضوعية: |
interleukin-33, ST2, septic arthritis, Staphylococcus aureus, interferon-γ, nitric oxide, Immunologic diseases. Allergy, RC581-607 |
| الوصف: |
The ST2 receptor is a member of the Toll/IL-1R superfamily and interleukin-33 (IL-33) is its agonist. Recently, it has been demonstrated that IL-33/ST2 axis plays key roles in inflammation and immune mediated diseases. Here, we investigated the effect of ST2 deficiency in Staphylococcus aureus-induced septic arthritis physiopathology. Synovial fluid samples from septic arthritis and osteoarthritis individuals were assessed regarding IL-33 and soluble (s) ST2 levels. The IL-33 levels in samples from synovial fluid were significantly increased, whereas no sST2 levels were detected in patients with septic arthritis when compared with osteoarthritis individuals. The intra-articular injection of 1 × 107 colony-forming unity/10 μl of S. aureus American Type Culture Collection 6538 in wild-type (WT) mice induced IL-33 and sST2 production with a profile resembling the observation in the synovial fluid of septic arthritis patients. Data using WT, and ST2 deficient (−/−) and interferon-γ (IFN-γ)−/− mice showed that ST2 deficiency shifts the immune balance toward a type 1 immune response that contributes to eliminating the infection due to enhanced microbicide effect via NO production by neutrophils and macrophages. In fact, the treatment of ST2−/− bone marrow-derived macrophage cells with anti-IFN-γ abrogates the beneficial phenotype in the absence of ST2, which confirms that ST2 deficiency leads to IFN-γ expression and boosts the bacterial killing activity of macrophages against S. aureus. In agreement, WT cells achieved similar immune response to ST2 deficiency by IFN-γ treatment. The present results unveil a previously unrecognized beneficial effect of ST2 deficiency in S. aureus-induced septic arthritis. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
1664-3224 |
| Relation: |
http://journal.frontiersin.org/article/10.3389/fimmu.2018.00962/full; https://doaj.org/toc/1664-3224 |
| DOI: |
10.3389/fimmu.2018.00962 |
| URL الوصول: |
https://doaj.org/article/52348734dbfe400ebba3dcdfa2430d0b |
| رقم الانضمام: |
edsdoj.52348734dbfe400ebba3dcdfa2430d0b |
| قاعدة البيانات: |
Directory of Open Access Journals |
Full Text Finder