CXCL8 (interleukin 8) – the key inflammatory mediator in chronic obstructive pulmonary disease?

Chronic obstructive pulmonary disease (COPD) is a prevalent chronic disease of the upper airways and it is the fourth cause of death in the Polish population. COPD is characterized by not fully reversible constriction of air flow, which is a consequence of inflammation caused by noxious fumes and gases, particularly tobacco smoke. It seems that among mediators of inflammation, chemokine CXCL8 (interleukin 8) may play a pivotal role. CXCL8 is a member of the chemokine family and is a major chemoattractant to neutrophils, which are responsible for inducing and sustaining the inflammatory state. It was shown that there is a correlation between the number of neutrophils in induced sputum in COPD patients, the CXCL8 level, and clinical outcome of the illness. Increased frequency of exacerbation may be a result of increased secretion of mucus caused by increased expression of genes encoding mucins (MUC5AC and MUCB), which is stimulated by high levels of CXCL8. Activation of the CXCL8-encoding gene depends on pro-inflammatory cytokines such as tumor necrosis factor, interleukin 1 and lipopolysaccharide which activate transcription factor NF-κB. Inhibitors of CXCL8 (such as N-acetyl-L-cysteine) cause a decrease of exacerbation frequency and clinical symptoms. The data presented in the review suggest that CXCL8 plays a major role in the inflammatory process leading to COPD.