Details

Autor(en) / Beteiligte

• Staurengo-Ferrari, Larissa
• Trevelin, Silvia C
• Fattori, Victor
• Nascimento, Daniele C
• de Lima, Kalil A
• Pelayo, Jacinta S
• Figueiredo, Florêncio
• Casagrande, Rubia
• Fukada, Sandra Y
• Teixeira, Mauro M
• Cunha, Thiago M
• Liew, Foo Y
• Oliveira, Rene D
• Louzada-Junior, Paulo
• Cunha, Fernando Q
• Alves-Filho, José C
• Verri, Waldiceu A

Titel

Interleukin-33 Receptor (ST2) Deficiency Improves the Outcome of Staphylococcus aureus -Induced Septic Arthritis

Ist Teil von

• Frontiers in immunology, 2018-05, Vol.9, p.962-962

Ort / Verlag

Switzerland: Frontiers Research Foundation

Erscheinungsjahr

2018

Link zum Volltext

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 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 -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 × 10  colony-forming unity/10 μl of 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 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 . 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 -induced septic arthritis.