Hepcidin expression and iron transport in alveolar macrophages.

@article{Nguyen2006HepcidinEA,
  title={Hepcidin expression and iron transport in alveolar macrophages.},
  author={Ngoc B. Nguyen and Kimberly D. Callaghan and Andrew J. Ghio and David J. Haile and Funmei Yang},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2006},
  volume={291 3},
  pages={
          L417-25
        }
}
Alveolar macrophages express many proteins important in iron homeostasis, including the iron importer divalent metal transport 1 (DMT1) and the iron exporter ferroportin 1 (FPN1) that likely participate in lung defense. We found the iron regulatory hormone hepcidin (HAMP) is also produced by alveolar macrophages. In mouse alveolar macrophages, HAMP mRNA was detected at a low level when not stimulated but at a high level when exposed to lipopolysaccharide (LPS). LPS also affected the mRNA levels… 
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It is concluded that hepcidin expression in macrophages is regulated mainly through TLR2 and TLR4 receptors via the MyD88-dependent signaling pathway and that autocrine regulation of iron accumulation inmacrophages by hePCidin may affect the levels of proinflammatory cytokine production.
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It is demonstrated that differentiated human airway epithelial cells express hepcidin mRNA and that its expression is augmented in response to IFN-γ via activation of STAT1.
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Iron modulates the inflammatory response outcome, as elevated iron levels increased M2 phenotype and negatively regulated M1 proinflammatory LPS-induced response.
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