Variation in Iron Homeostasis Genes Between Patients With ARDS and Healthy Control Subjects

Lagan, Anna L.; Quinlan, Gregory J.; Mumby, Sharon; Melley, Daniel D.; Goldstraw, Peter; Bellingan, Geoff; Hill, Michael; Briggs, David; Pantelidis, Panagiotis; Bois, Roland M. du; Welsh, Kenneth I.; Evans, Timothy W.

doi:10.1378/chest.07-1117

Cited by 32 publications

(20 citation statements)

References 57 publications

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“…25,26 In addition, polymorphisms within the gene that encodes the ferritin light chain are associated with the development of ARDS. 27 Thus, altered intracellular and extracellular ferritin expression may have implications in the development of lung inflammation, including ARDS. Consistent with our results, a recent study reported that epithelial cells treated with carbon monoxide (CO) gas, which has a high affinity for ferrous iron and can alter iron metabolism in bronchial epithelial cells, 28 exhibited a decreased ferritin concentration.…”

Section: Discussionmentioning

confidence: 99%

Serum ferritin and transferrin levels as serologic markers of methylene diphenyl diisocyanate–induced occupational asthma

Hur

Choi

Sheen

et al. 2008

Journal of Allergy and Clinical Immunology

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Background: Although methylene diphenyl diisocyanate (MDI) may induce occupational asthma in the workplace, the pathogenic mechanisms are unclear. Objectives: By using bronchoalveolar lavage fluid, we sought to identify proteins that were differentially expressed between subjects with MDI-induced occupational asthma (MDI-OA) and asymptomatic exposed controls (AECs). Methods: To find proteins that were differentially expressed between the MDI-OA and AEC groups, 2-dimensional electrophoresis was performed by using bronchoalveolar lavage fluid obtained from subjects after MDI-specific inhalation challenge. The selected protein spots were then identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The clinical relevance of the differentially expressed spots was compared by ELISA using sera from the MDI-OA/eosinophilic bronchitis, AEC, and unexposed healthy control groups. Receiver operating characteristic curves were then plotted, and the sensitivity and specificity were determined. Results: Twenty-three protein spots were identified that distinguished the subjects with MDI-OA from those in the AEC group. Among them, ferritin expression was downregulated whereas transferrin expression was upregulated in subjects with MDI-OA compared with AEC; these results were validated by ELISA using sera from the MDI-OA/EB and AEC groups. To identify subjects with MDI-OA, the optimal serum cutoff levels were 69.84 ng/mL for ferritin and 2.48 mg/mL for transferrin. When these 2 parameters were combined, the sensitivity was 71.43% and the specificity was 85.71%. Conclusion: Serum ferritin and transferrin levels are associated with the phenotype of MDI-OA. (J Allergy Clin Immunol 2008;122:774-80.)

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Section: Discussionmentioning

confidence: 99%

Serum ferritin and transferrin levels as serologic markers of methylene diphenyl diisocyanate–induced occupational asthma

Hur

Choi

Sheen

et al. 2008

Journal of Allergy and Clinical Immunology

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“…After the first gene in regulating oxidant-mediated response in ALI-transcription factor NRF2 was reported (63), two additional genes in oxidant/antioxidant pathway were reported (SOD3/EC-SOD and NQO1) (8,78). altered iron handling (i.e., excessive iron-catalyzed oxidative stress) may also play a role in ALI (52). A detailed summary of these candidate genes associated with lung injury is presented here.…”

Section: Established Genetic Associations In Lung Injury: a Pathway-omentioning

confidence: 96%

Recent advances in genetic predisposition to clinical acute lung injury

Gao¹,

Barnes²

2009

American Journal of Physiology-Lung Cellular and Molecular Phys

100

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“…The combined actions of SOD and H 2 O 2 -metabolizing enzymes maintain low overall steadystate levels of O 2 À and H 2 O 2 and prevent unwanted actions of these ROS while allowing for appropriate localized ROS-mediated redox signaling by, for example, NOX enzymes. Furthermore, since these primary ROS can also react with available redox-active transition metals to produce the highly reactive hydroxyl radical (OH ) (Cross et al, 1994), homeostasis of these transition metals must be carefully regulated, and alterations in iron homeostasis genes in various lung pathologies (Ghio, 2009;Lagan et al, 2008) may contribute to ROS-dependent injury in these cases. Additional enzymatic antioxidant systems include thioredoxins (Trx) and glutaredoxins (GRX), which act primarily by reversing protein cysteine oxidation, enzymes involved in synthesis or maintenance of the low-molecular-weight thiol glutathione (GSH) as a critical cofactor for GPX or GRX, and other enzymes such as heme oxygenase and metallothionein, which are thought to contribute to antioxidant defense by more indirect mechanisms.…”

Section: Antioxidant Defenses In the Lungmentioning

confidence: 99%

Antioxidant Defenses in the Lung

Vliet¹

2015

Comparative Biology of the Normal Lung

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Variation in Iron Homeostasis Genes Between Patients With ARDS and Healthy Control Subjects

Cited by 32 publications

References 57 publications

Serum ferritin and transferrin levels as serologic markers of methylene diphenyl diisocyanate–induced occupational asthma

Serum ferritin and transferrin levels as serologic markers of methylene diphenyl diisocyanate–induced occupational asthma

Recent advances in genetic predisposition to clinical acute lung injury

Antioxidant Defenses in the Lung

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