Iron metabolism is of crucial importance in the biology and pathophysiology of the lower respiratory tract. As with many other factors involved in inflammation, it is very important that an appropriate iron balance is maintained. Local deficiency could impair growth and proliferation of cells responsible for the inflammatory response and tissue repair (lymphocytes and fibroblasts) and the synthesis of mediators (for example, arachidonic acid derivatives).1 In contrast, excessive accumulation of iron, especially in free form—that is, not bound to one of the specific iron-binding proteins—facilitates the generation of potentially toxic hydroxyl radicals2 and increases the ability of intracellular bacteria such as mycobacteria to grow.3-5

Research into iron metabolism in the lower respiratory tract has taken advantage of bronchoalveolar lavage, a technique by which it is possible to obtain the cells and fluid lining the alveoli. Determination of iron content in the alveolo-interstitial region shows that 80% is present in the cells and 20% in the epithelial lining fluid of the lung.6 Since alveolar macrophages constitute the major cell population in this region, and because the iron content of lymphocytes, neutrophils, and monocytes is very low in comparison with alveolar macrophages,6 ,7 these cells are of special interest.

In this paper we review current knowledge of iron and iron-binding proteins in bronchoalveolar lavage fluid, and the special features of iron metabolism in alveolar macrophages.