Cytokines and therapy in COPD: a promising combination?
COPD is a major health problem, with patients showing a progressively declining, largely irreversible, change in lung function. This is associated with chronic airways inflammation and structural remodeling, including loss of alveolar walls, and goblet cell metaplasia with mucus hypersecretion. Inflammatory cells may contribute to the airway remodeling via secretion of proteases, fibrotic or mitogenic growth factors, and cytokines. In turn, airway remodeling may contribute to the clinical symptoms of COPD. Currently available therapies are directed to improvement of clinical symptoms and reduction of the airways inflammation. The commonly used glucocorticosteroids are expected to reduce the inflammation by acting on kinases or transcription factors necessary for expression of pro-inflammatory cytokines or chemokines. However, several long-term and short-term studies showed that glucocorticosteroids are rather ineffective in improving lung function and reducing the airway inflammation in patients with COPD. New therapeutic strategies may reduce the inflammation and alleviate the clinical symptoms of COPD. Tumor necrosis factor-alpha, interleukin-8, and monocyte chemoattractant protein-1 are important chemotactic proteins for macrophages and neutrophils, the predominant inflammatory cells associated with COPD. As lung levels of these cytokines are higher in COPD compared to non-COPD patients, they may represent targets for novel therapies.
|Keywords||Animals, Cytokines/*antagonists & inhibitors/immunology, Glucocorticoids/pharmacology, Humans, Interleukin-8/antagonists & inhibitors/immunology, Monocyte Chemoattractant Protein-1/antagonists & inhibitors/immunology, Pulmonary Disease, Chronic Obstructive/*drug therapy/immunology, Tumor Necrosis Factor-alpha/antagonists & inhibitors/immunology|
de Boer, W.I.. (2002). Cytokines and therapy in COPD: a promising combination?. Chest: the cardiopulmonary and critical care journal. Retrieved from http://hdl.handle.net/1765/9903