PMID- 31726018
OWN - NLM
STAT- MEDLINE
DCOM- 20200721
LR  - 20211204
IS  - 1535-4989 (Electronic)
IS  - 1044-1549 (Linking)
VI  - 62
IP  - 5
DP  - 2020 May
TI  - Effect of Iron Deficiency on a Murine Model of Smoke-induced Emphysema.
PG  - 588-597
LID - 10.1165/rcmb.2018-0239OC [doi]
AB  - Smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). 
      Smoking susceptibility is important for the onset and development of COPD. We 
      previously reported an association between serum iron concentrations and 
      pulmonary function in male smokers. However, the mechanism governing smoking 
      susceptibility in relation to iron deficiency is unclear; this study aimed to 
      elucidate this mechanism. C57BL/6 male mice were fed an iron-deficient or normal 
      diet and then exposed to cigarette smoke. BAL, histological analysis, and 
      pulmonary function tests were performed after cigarette smoke exposure. Human 
      alveolar type II epithelial A549 cells were treated with an iron chelator. 
      Subsequently, A549 cells were exposed to cigarette smoke extract. In mice exposed 
      to cigarette smoke for 2 weeks, the concentration of alveolar macrophages in the 
      BAL fluid recovered from iron-deficient mice was significantly higher than that 
      in normal diet mice. IL-6 and MCP-1 (monocyte chemotactic protein 1) 
      concentrations in the BAL fluid increased significantly from baseline in 
      iron-deficient mice, but not in normal diet mice. In mice exposed to cigarette 
      smoke for 8 weeks, the pathological mean linear intercepts, physiological total 
      lung capacity, and functional residual capacity in the lungs of iron-deficient 
      mice were significantly greater than in normal diet mice. Phosphorylation of 
      NF-kappaB was enhanced in the lungs of iron-deficient mice exposed to cigarette smoke 
      and in the iron-chelating A549 cells exposed to cigarette smoke extract. Iron 
      deficiency exaggerated cigarette smoke-induced pulmonary inflammation, suggesting 
      that it may accelerate COPD development.
FAU - Sato, Kento
AU  - Sato K
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Inoue, Sumito
AU  - Inoue S
AUID- ORCID: 0000-0002-1817-9761
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Igarashi, Akira
AU  - Igarashi A
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Tokairin, Yoshikane
AU  - Tokairin Y
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Yamauchi, Keiko
AU  - Yamauchi K
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Kimura, Tomomi
AU  - Kimura T
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Nishiwaki, Michiko
AU  - Nishiwaki M
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Nemoto, Takako
AU  - Nemoto T
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Nakano, Hiroshi
AU  - Nakano H
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Sato, Masamichi
AU  - Sato M
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Machida, Hiroyoshi
AU  - Machida H
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Yang, Sujeong
AU  - Yang S
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Minegishi, Yukihiro
AU  - Minegishi Y
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Furuyama, Kodai
AU  - Furuyama K
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Watanabe, Masafumi
AU  - Watanabe M
AD  - Department of Cardiology, Pulmonology, and Nephrology, Yamagata University 
      Faculty of Medicine, Yamagata, Japan; and.
FAU - Shibata, Yoko
AU  - Shibata Y
AUID- ORCID: 0000-0003-1794-0026
AD  - Department of Pulmonary Medicine, Fukushima Medical University, Fukushima, Japan.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Ions)
RN  - 0 (Iron Chelating Agents)
RN  - 0 (NF-kappa B)
RN  - E1UOL152H7 (Iron)
SB  - IM
CIN - Am J Respir Cell Mol Biol. 2020 May;62(5):541-542. PMID: 31743655
MH  - A549 Cells
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid
MH  - Diet
MH  - Dietary Supplements
MH  - Disease Models, Animal
MH  - Emphysema/blood/*etiology
MH  - Erythrocyte Count
MH  - Humans
MH  - Inflammation/blood/complications/pathology
MH  - Ions
MH  - Iron/blood
MH  - Iron Chelating Agents/pharmacology
MH  - *Iron Deficiencies
MH  - Lung/pathology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - Phosphorylation/drug effects
MH  - Smoking/*adverse effects
OTO - NOTNLM
OT  - chronic obstructive pulmonary disease
OT  - emphysema
OT  - iron deficiency
OT  - murine model
OT  - smoking
EDAT- 2019/11/15 06:00
MHDA- 2020/07/22 06:00
CRDT- 2019/11/15 06:00
PHST- 2019/11/15 06:00 [pubmed]
PHST- 2020/07/22 06:00 [medline]
PHST- 2019/11/15 06:00 [entrez]
AID - 10.1165/rcmb.2018-0239OC [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 2020 May;62(5):588-597. doi: 10.1165/rcmb.2018-0239OC.