Many inflammatory cells and mediators are involved in COPD inflammation, so there are many potential targets. However, treatments that are too specific or downstream may have little effect or target only a small proportion of patients (i.e. responder phenotypes), as demonstrated by single mediator antagonists that have proven ineffective, including tumour necrosis factor-α, interleukin (IL)-1β, and IL-5 blocking antibodies [154, 155].