Tumour necrosis factor-α blockade suppresses murine allergic airways inflammation

摘要: Asthma is a heterogeneous disease that has been increasing in incidence throughout western societies and cytokines, including proinflammatory tumour necrosis factor alpha (TNF-alpha), have implicated the pathogenesis of asthma. Anti-TNF-alpha therapies established successfully clinic for diseases such as rheumatoid arthritis Crohn's disease. TNF-alpha-blocking strategies are now being trialled asthma; however, their mode action poorly understood. Based on observation TNF-alpha induces lymph node hypertrophy we attempted to investigate this mechanism airway inflammation by employing two models murine inflammation, termed short long models, representing severe mild/moderate asthma, respectively. The differ immunization schedules. In model, characterized eosinophilic neutrophilic effect blockade was reduction draining (DLN) hypertrophy, eosinophilia, interleukin (IL)-5 production immunoglobulin E (IgE) production. produced DLN IL-5 but had limited effects eosinophilia IgE These results indicate anti-TNF-alpha can suppress decrease inflammation. Further investigations showed anti-TNF-alpha-induced inhibition cannot be explained preventing l-selectin-dependent capture lymphocytes into DLN. Given overall TNF able model (severe) more effectively than (mild/moderate), suggest blocking may effective treatment