Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory condition, characterised by progressive, irreversible airflow obstruction. The major risk factor for development of COPD is cigarette smoking, and the disease is predicted to become the 3rd leading cause of death by 2020. Currently, there are no pharmacological interventions that halt the progression of COPD; however one strategy is to reduce the chronic lung inflammation associated with this disease. An increased inflammatory infiltrate comprising macrophages, neutrophils and T-lymphocytes is a major hallmark of COPD. Furthermore, both macrophages and neutrophils have the ability to cause all the pathological changes associated with COPD. Chemokines that are elevated in sputum from COPD patients have the capacity to recruit neutrophils, the macrophage precursor cells, monocytes, and T-lymphocytes. Chemokines are considered predominantly chemotactic cytokines however; there is a growing body of evidence demonstrating that chemokines can also act as functional antagonists thus leading to selective recruitment of inflammatory cells. Whilst inhibition of chemokine dependent recruitment of inflammatory cells via small molecule antagonists gives rise to potential treatments for COPD, the discovery that chemokines are also natural antagonists could also be exploited in the ongoing search for treatment of this currently fatal disease.
Keywords: copd, chemokines, receptors, therapeutics, cxcr2, cxcr3
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