Iron metabolism in the lower respiratory tract
Open accessAbstract
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. Iron is principally required for haemoglobin synthesis, and its uptake, utilisation and storage are carefully regulated to ensure an adequate supply without excessive accumulation which could lead to toxicity. Intestinal iron absorption is related to erythropoietic requirements, although the regulatory mechanism(s) remain unknown. The usual source of iron in the lung is serum iron which is derived from catabolised erythrocytes and absorbed iron. However, in pathological states, iron can enter the lung …
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Many particles associated with smoking are heavily laden with micro-particulate iron, which is a substantial contributor to disease as a major catalyst of hydroxyl radical production.
“many of the particles associated with smoking (and also ingested from other sources) are heavily laden with micro-particulate iron, which, as a major catalyst of hydroxyl radical production, undoubtedly is a substantial contributor as well (see e.g. [1373,1384,1396-1400]).”
From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [1398]
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- Authors
- Mateos, F., Brock, J. H., & Perez-Arellano, J. L.
- Affiliations
- Universidad de Las Palmas de Gran Canaria (ES)
- Venue
- Thorax
- Publisher
- BMJ
- Published
- 1998-07-01
- Volume
- 53
- Issue
- 7
- Pages
- 594-600
- ISSN
- 0040-6376 (ISSN-L)
- PMC
- PMC1745270
- OpenAlex
- W2162214744
- Cited by
- 158
- References
- 70
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 5 · 2023: 5 · 2022: 5 · 2021: 6 · 2020: 6 · 2019: 2 · 2018: 2 · 2017: 8 · 2016: 4 · 2015: 5 · 2014: 10 · 2013: 5 · 2012: 5
- FWCI
- 1.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Thorax (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Keywords
- iron metabolism, lower respiratory tract, bronchoalveolar lavage, iron-binding proteins, alveolar macrophages, free iron, oxidative stress, hydroxyl radicals, iron deficiency, iron overload, inflammation, tissue repair, epithelial lining fluid, mycobacterial growth
- MeSH terms
- Bronchi, Bronchoalveolar Lavage Fluid, Humans, Iron, Lactoferrin, Lung Diseases, Pulmonary Alveoli, Smoking, Transferrin, Macrophages, Alveolar
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