Iron metabolism in the lower respiratory tract

Mateos, Fernando; Brock, Jeremy H.; Pérez-Arellano, José Luís

doi:10.1136/thx.53.7.594

Cited by 147 publications

(113 citation statements)

References 56 publications

(45 reference statements)

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“…The total amount of iron in the alveolar macrophages can be quantified using cytochemical (Perls), colorimetric (ferrozine), or particle-induced X-ray emission techniques [62,63]. The iron sources in the lungs are: circulatory, where it is bound to transferrin or lactoferrin, inhalatory (from cigarette smoke or metallic dusts); or from the red cell metabolism during episodes of alveolar haemorrhage.…”

Section: Metabolic Theorymentioning

confidence: 99%

“…The iron sources in the lungs are: circulatory, where it is bound to transferrin or lactoferrin, inhalatory (from cigarette smoke or metallic dusts); or from the red cell metabolism during episodes of alveolar haemorrhage. Transferrin is capable of providing iron only to cells that express CD71, or transferrin receptors, such as B and T lymphocytes and alveolar macrophages [62,64,65].…”

Section: Metabolic Theorymentioning

confidence: 99%

“…Concomitantly with acute iron overload there is a significant increase in the alveolar macrophages synthesis of L (light)-type isoferritin, which, by an unknown mechanism, escapes into the systemic circulation, possibly by alveolar macrophage death or as a lymphocytic source [67]; furthermore, this amount of plasma ferritin does not seem to correlate with total-body iron deficiency status in IPH [68]. Also, the alveolar macrophage apparatus is easily exhaustible, and free iron can be present in the alveoli, leading eventually to pulmonary fibrosis [62,69,70]. One of the proposed toxic mechanism of the free iron ion against the pulmonary residing cells is thought to be related to its capacity to produce highly reactive hydroxyl radicals from less toxic oxygen superoxide and hydrogen peroxide, leading ultimately to lipid layer peroxidation, protein and carbohydrate degradation, and stimulation of fibrogenesis.…”

Section: Metabolic Theorymentioning

confidence: 99%

See 2 more Smart Citations

Idiopathic pulmonary haemosiderosis revisited

Ioachimescu¹,

Sieber²,

Kotch³

2004

European Respiratory Journal

205

199

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Idiopathic pulmonary haemosiderosis is a rare cause of diffuse alveolar haemorrhage of unknown aetiology. It occurs most frequently in children, has a variable natural history with repetitive episodes of diffuse alveolar haemorrhage, and has been reported to have a high mortality. Many patients develop iron deficiency anaemia secondary to deposition of haemosiderin iron in the alveoli.Examination of sputum and bronchoalveolar lavage fluid can disclose haemosiderinladen alveolar macrophages (siderophages), and the lung biopsy shows numerous siderophages in the alveoli, without any evidence of pulmonary vasculitis, nonspecific/ granulomatous inflammation, or deposition of immunoglobulins. Contrary to earlier reports, corticosteroids alone or in combination with other immunosuppressive agents may be effective for either exacerbations or maintenance therapy of idiopathic pulmonary haemosiderosis.

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Section: Metabolic Theorymentioning

confidence: 99%

Section: Metabolic Theorymentioning

confidence: 99%

Section: Metabolic Theorymentioning

confidence: 99%

See 1 more Smart Citation

Idiopathic pulmonary haemosiderosis revisited

Ioachimescu¹,

Sieber²,

Kotch³

2004

European Respiratory Journal

205

199

View full text Add to dashboard Cite

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“…18,19 The generation of ROS in epithelial lining fluid may be further enhanced by the presence of increased amounts of free iron in the pulmonary airspaces in smokers. 20,21 This is relevant to COPD since the intracellular iron content of alveolar macrophages is augmented in cigarette smokers and is further increased in those who develop chronic bronchitis, compared with non-smokers. 22 In addition, macrophages obtained from smokers release more free iron in vitro than those from non-smokers.…”

Section: Sources Of Ros In the Lungmentioning

confidence: 99%

Glutathione peroxidase-1 as a novel therapeutic target for COPD

Vlahos

Bozinovski

2013

Redox Report

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Oxidative stress plays a role in a variety of diseases but it is even more pertinent in chronic obstructive pulmonary disease (COPD) given the increased oxidant burden in smokers. The increased oxidant burden results from the fact that cigarette smoke contains over 4700 different chemical compounds and more than 10 15 oxidants/free radicals per puff. Other factors, such as air pollutants, infections, and occupational dusts that may exacerbate COPD, also have the potential to produce oxidative stress. These oxidants give rise to Reactive Oxygen Species (ROS) that are generated enzymatically by inflammatory and epithelial cells within the lung as part of an inflammatory immune response towards a pathogen or irritant. Thus, while ROS are necessary for host defence against invading pathogens, increased levels of ROS have been implicated in initiating inflammatory responses in the lungs through the activation of transcriptional factors, signal transduction pathways, chromatin remodelling and gene expression of proinflammatory mediators. However, the normal lung has developed defences to ROS-mediated damage, which include antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. In this review we consider the therapeutic potential of the antioxidant enzyme glutathione peroxidase-1 for the treatment of cigarette smoke-induced lung inflammation and damage.

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“…Transferrin (Tf) is a major iron-binding glycoprotein with a molecular weight of 79500 Da [1,2]. Tf also plays essential roles in iron-binding and -transport, antimicrobial activity, cell growth, cell differentiation and cytoprotective processes [3,4].…”

Section: Introductionmentioning

confidence: 99%

Levels of Transferrin in Bronchoalveolar Lavage Fluid in Sarcoidosis

Shigemura

Nasuhara

Konno

et al. 2010

Lung

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There has been only one report showing high levels of transferrin (Tf) in bronchoalveolar lavage fluid (BALF) in patients with sarcoidosis. The aim of this study is to assess the levels of Tf in both BALF and serum and to examine the relationship between the levels of Tf and other disease markers in sarcoidosis.Subjects were 64 sarcoidosis and 10 healthy controls. Tf in BALF and serum was measured by nephelometric assay. Median Tf levels in BALF from sarcoidosis was 0.70 mg/dl (range, 0.00-3.97), which was significantly higher when compared with controls (0.36 mg/dl; range, 0.00-1.02) (p=0.005). In contrast, median Tf levels in serum from sarcoidosis was 258 mg/dl (range, 171-383), which was significantly lower when compared with controls (322 mg/dl; range, 234-356) (p=0.003). Tf levels in BALF were significantly correlated with both the percentage of lymphocytes (r=0.617, p=0.001) and serum angiotensin-converting enzyme activity (r=0.363, p=0.003) and serum soluble interleukin-2 receptor (r=0.450, p=0.001) in sarcoidosis. Levels of Tf in BALF from patients with sarcoidosis were not influenced by smoking status. The levels of Tf in sarcoidosis are high in BALF, but low in serum. Increased levels of Tf in BALF may reflect the disease activity.

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Iron metabolism in the lower respiratory tract

Cited by 147 publications

References 56 publications

Idiopathic pulmonary haemosiderosis revisited

Idiopathic pulmonary haemosiderosis revisited

Glutathione peroxidase-1 as a novel therapeutic target for COPD

Levels of Transferrin in Bronchoalveolar Lavage Fluid in Sarcoidosis

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