作者: Marina C Oliveira , Luciana P Tavares , Juliana P Vago , Nathália V Batista , Celso M Queiroz-Junior
DOI: 10.1371/JOURNAL.PONE.0146403
关键词: Endocrinology 、 Etanercept 、 PTX3 、 Inflammation 、 Receptor antagonist 、 Drug metabolism 、 Tumor necrosis factor alpha 、 Adipokine 、 Arthritis 、 Immunology 、 Medicine 、 Internal medicine
摘要: Metabolic alterations are associated with arthritis apart from obesity. However, it is still unclear which the underlying process behind these metabolic changes. Here, we investigate role of tumor necrosis factor (TNF) in this an acute model antigen-induced (AIA). Immunized male BALB/c mice received intra-articular injection PBS (control) or methylated bovine serum albumin (mBSA) into their knees, and were also pre-treated different drugs: Etanercept, anti-TNF drug, DF2156A, a CXCR1/2 receptor antagonist, monoclonal antibody RB6-8C5 to deplete neutrophils. Local challenge mBSA evoked neutrophil influx knee joint, enhanced joint nociception, along transient systemic alteration (higher levels glucose lipids, altered adipocytokines). Pre-treatment conventional biological inhibitor TNF action, ameliorated nociception inflammation dominated by neutrophils, markedly improved many metabolites (glucose lipids), adipocytokines PTX3. lessening changes was not due diminished accumulation neutrophils Etanercept. Reduction recruitment pre-treating AIA even depletion cells using reduced all inflammatory parameters hypernociception developed after challenge, but could prevent Therefore, induction provoked involved TNF. We suggest that arthritis-associated local major present model, rather cytokines.