Hepcidin Is Essential for Alveolar Macrophage Function and Is Disrupted by Smoke in a Murine Chronic Obstructive Pulmonary Disease Model.
Animals
Bone Marrow
/ metabolism
Cation Transport Proteins
/ metabolism
Cigarette Smoking
/ metabolism
Disease Models, Animal
Disease Progression
Erythropoietin
/ metabolism
Hepcidins
/ metabolism
Humans
Iron
/ metabolism
Lung
/ metabolism
Macrophages, Alveolar
/ metabolism
Mice
Mice, Inbred C57BL
Peptides
/ metabolism
Pulmonary Disease, Chronic Obstructive
/ metabolism
Smoke
Smoking
/ metabolism
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
01 11 2020
01 11 2020
Historique:
received:
23
10
2019
accepted:
31
08
2020
pubmed:
23
9
2020
medline:
7
4
2021
entrez:
22
9
2020
Statut:
ppublish
Résumé
Chronic obstructive pulmonary disease (COPD) is a debilitating lung disease associated with cigarette smoking. Alterations in local lung and systemic iron regulation are associated with disease progression and pathogenesis. Hepcidin, an iron regulatory peptide hormone, is altered in subjects with COPD; however, the molecular role of hepcidin in COPD pathogenesis remains to be determined. In this study, using a murine model of smoke-induced COPD, we demonstrate that lung and circulating hepcidin levels are inhibited by cigarette smoke. We show that cigarette smoke exposure increases erythropoietin and bone marrow-derived erythroferrone and leads to expanded but inefficient erythropoiesis in murine bone marrow and an increase in ferroportin on alveolar macrophages (AMs). AMs from smokers and subjects with COPD display increased expression of ferroportin as well as hepcidin. Notably, murine AMs exposed to smoke fail to increase hepcidin in response to Gram-negative or Gram-positive infection. Loss of hepcidin in vivo results in blunted functional responses of AMs and exaggerated responses to
Identifiants
pubmed: 32958690
pii: jimmunol.1901284
doi: 10.4049/jimmunol.1901284
pmc: PMC7805484
mid: NIHMS1626305
doi:
Substances chimiques
Cation Transport Proteins
0
Hepcidins
0
Peptides
0
Smoke
0
metal transporting protein 1
0
Erythropoietin
11096-26-7
Iron
E1UOL152H7
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2489-2498Subventions
Organisme : NHLBI NIH HHS
ID : R00 HL125899
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG052530
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG056699
Pays : United States
Organisme : Department of Health
Pays : United Kingdom
Informations de copyright
Copyright © 2020 by The American Association of Immunologists, Inc.
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