Decreased breath excretion of redox active iron in COPD: a protective failure?

Recent observational and genetic studies have highlighted a potential role for disrupted iron homeostasis in stable and exacerbating chronic obstructive pulmonary disease (COPD). Thus iron deficiency that is not limited to anaemia [1] and single nucleotide polymorphism in the gene encoding iron regulatory protein-2 [2], a key regulatory factor involved in cellular iron turnover and control, have been identified in this population. Disrupted systemic iron homeostasis is likely to limit iron availability for metabolic purposes due to overriding effects on tissue storage rather than on mobilisation and limitation of uptake from the gut. A specific pro-oxidant pool of iron (free or loosely bound ions, which are redox active/catalytic for damaging oxidant production) is measurable in exhaled breath condensate (EBC) [3]. While iron is essential for life, particularly for aerobes, poor or altered iron handling results in adverse effects related to oxidant production, microbial virulence, altered redox signalling events and altered cellular fate, including remodelling. This study was therefore undertaken to gain insight into iron handling in lungs and airways, and the extent to which these processes may be altered in COPD. Studies were undertaken to measure this specific iron pool by the bleomycin method [4] utilising EBC samples collected as previously described [3] and obtained from normal healthy individuals, healthy smokers and patients with COPD (current and ex-smokers). Serum levels of hepcidin and interleukin (IL)-6, known regulators of iron homeostasis, were also measured.