Aging affects lipopolysaccharide-induced upregulation of heme oxygenase-1 in the lungs and alveolar macrophages

Yoko Ito, Tomoko Betsuyaku, Chinatsu Moriyama, Yasuyuki Nasuhara, Masaharu Nishimura

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Lung injuries are generally more serious and cause high mortality in aged humans and animals. Heme Oxygenase-1 (HO-1) is known to be readily inducible in alveolar macrophages (AMs) and airway epithelial cells to confer cytoprotection against oxidative stress. We thus investigated whether aging impairs the stress-induced upregulation of HO-1. In this study, we first quantified basal levels of HO-1 expression in lungs from male ICR mice of various ages. Second, young (9-11 weeks) and old (65-66 weeks) mice were subjected to intratracheal administration of lipopolysaccharide (LPS) and expression of HO-1 in the lungs was quantified at 2, 24 and 72 h. HO-1 expression in bronchiolar epithelial cells harvested by laser capture microdissection (LCM) was also specifically quantified in the two age groups. Third, we examined HO-1 expression in AMs lavaged from 22-week-old and 86-96-week-old male ICR mice in response to LPS for 24 h in vitro. We found that basal expression of HO-1 in the lungs did not differ with age. LPS-induced HO-1 upregulation was significantly impaired in the lungs of 65-66-week-old mice than in 9-11-week-old mice at 2 and 24 h, although there were no differences in the magnitude of HO-1 upregulation in bronchiolar epithelium at 2 h. LPS-induced upregulation of HO-1 was observed in AMs from 22-week-old mice (1.8-fold), but not in AMs from 86-96-week-old mice in vitro. In summary, we demonstrated age-related defects in HO-1 induction in the whole lungs and in AMs in response to LPS.

Original languageEnglish
Pages (from-to)173-180
Number of pages8
JournalBiogerontology
Volume10
Issue number2
DOIs
Publication statusPublished - 2009
Externally publishedYes

Fingerprint

Heme Oxygenase-1
Alveolar Macrophages
Lipopolysaccharides
Up-Regulation
Lung
Inbred ICR Mouse
Epithelial Cells
Laser Capture Microdissection
Cytoprotection
Lung Injury
Oxidative Stress
Epithelium
Age Groups

Keywords

  • Acute lung injury
  • Aging
  • HO-1
  • LPS

ASJC Scopus subject areas

  • Geriatrics and Gerontology
  • Gerontology
  • Ageing

Cite this

Aging affects lipopolysaccharide-induced upregulation of heme oxygenase-1 in the lungs and alveolar macrophages. / Ito, Yoko; Betsuyaku, Tomoko; Moriyama, Chinatsu; Nasuhara, Yasuyuki; Nishimura, Masaharu.

In: Biogerontology, Vol. 10, No. 2, 2009, p. 173-180.

Research output: Contribution to journalArticle

Ito, Yoko ; Betsuyaku, Tomoko ; Moriyama, Chinatsu ; Nasuhara, Yasuyuki ; Nishimura, Masaharu. / Aging affects lipopolysaccharide-induced upregulation of heme oxygenase-1 in the lungs and alveolar macrophages. In: Biogerontology. 2009 ; Vol. 10, No. 2. pp. 173-180.
@article{2fb6c96a5a7143c9b901f2d9ab5827b6,
title = "Aging affects lipopolysaccharide-induced upregulation of heme oxygenase-1 in the lungs and alveolar macrophages",
abstract = "Lung injuries are generally more serious and cause high mortality in aged humans and animals. Heme Oxygenase-1 (HO-1) is known to be readily inducible in alveolar macrophages (AMs) and airway epithelial cells to confer cytoprotection against oxidative stress. We thus investigated whether aging impairs the stress-induced upregulation of HO-1. In this study, we first quantified basal levels of HO-1 expression in lungs from male ICR mice of various ages. Second, young (9-11 weeks) and old (65-66 weeks) mice were subjected to intratracheal administration of lipopolysaccharide (LPS) and expression of HO-1 in the lungs was quantified at 2, 24 and 72 h. HO-1 expression in bronchiolar epithelial cells harvested by laser capture microdissection (LCM) was also specifically quantified in the two age groups. Third, we examined HO-1 expression in AMs lavaged from 22-week-old and 86-96-week-old male ICR mice in response to LPS for 24 h in vitro. We found that basal expression of HO-1 in the lungs did not differ with age. LPS-induced HO-1 upregulation was significantly impaired in the lungs of 65-66-week-old mice than in 9-11-week-old mice at 2 and 24 h, although there were no differences in the magnitude of HO-1 upregulation in bronchiolar epithelium at 2 h. LPS-induced upregulation of HO-1 was observed in AMs from 22-week-old mice (1.8-fold), but not in AMs from 86-96-week-old mice in vitro. In summary, we demonstrated age-related defects in HO-1 induction in the whole lungs and in AMs in response to LPS.",
keywords = "Acute lung injury, Aging, HO-1, LPS",
author = "Yoko Ito and Tomoko Betsuyaku and Chinatsu Moriyama and Yasuyuki Nasuhara and Masaharu Nishimura",
year = "2009",
doi = "10.1007/s10522-008-9164-4",
language = "English",
volume = "10",
pages = "173--180",
journal = "Biogerontology",
issn = "1389-5729",
publisher = "Springer Netherlands",
number = "2",

}

TY - JOUR

T1 - Aging affects lipopolysaccharide-induced upregulation of heme oxygenase-1 in the lungs and alveolar macrophages

AU - Ito, Yoko

AU - Betsuyaku, Tomoko

AU - Moriyama, Chinatsu

AU - Nasuhara, Yasuyuki

AU - Nishimura, Masaharu

PY - 2009

Y1 - 2009

N2 - Lung injuries are generally more serious and cause high mortality in aged humans and animals. Heme Oxygenase-1 (HO-1) is known to be readily inducible in alveolar macrophages (AMs) and airway epithelial cells to confer cytoprotection against oxidative stress. We thus investigated whether aging impairs the stress-induced upregulation of HO-1. In this study, we first quantified basal levels of HO-1 expression in lungs from male ICR mice of various ages. Second, young (9-11 weeks) and old (65-66 weeks) mice were subjected to intratracheal administration of lipopolysaccharide (LPS) and expression of HO-1 in the lungs was quantified at 2, 24 and 72 h. HO-1 expression in bronchiolar epithelial cells harvested by laser capture microdissection (LCM) was also specifically quantified in the two age groups. Third, we examined HO-1 expression in AMs lavaged from 22-week-old and 86-96-week-old male ICR mice in response to LPS for 24 h in vitro. We found that basal expression of HO-1 in the lungs did not differ with age. LPS-induced HO-1 upregulation was significantly impaired in the lungs of 65-66-week-old mice than in 9-11-week-old mice at 2 and 24 h, although there were no differences in the magnitude of HO-1 upregulation in bronchiolar epithelium at 2 h. LPS-induced upregulation of HO-1 was observed in AMs from 22-week-old mice (1.8-fold), but not in AMs from 86-96-week-old mice in vitro. In summary, we demonstrated age-related defects in HO-1 induction in the whole lungs and in AMs in response to LPS.

AB - Lung injuries are generally more serious and cause high mortality in aged humans and animals. Heme Oxygenase-1 (HO-1) is known to be readily inducible in alveolar macrophages (AMs) and airway epithelial cells to confer cytoprotection against oxidative stress. We thus investigated whether aging impairs the stress-induced upregulation of HO-1. In this study, we first quantified basal levels of HO-1 expression in lungs from male ICR mice of various ages. Second, young (9-11 weeks) and old (65-66 weeks) mice were subjected to intratracheal administration of lipopolysaccharide (LPS) and expression of HO-1 in the lungs was quantified at 2, 24 and 72 h. HO-1 expression in bronchiolar epithelial cells harvested by laser capture microdissection (LCM) was also specifically quantified in the two age groups. Third, we examined HO-1 expression in AMs lavaged from 22-week-old and 86-96-week-old male ICR mice in response to LPS for 24 h in vitro. We found that basal expression of HO-1 in the lungs did not differ with age. LPS-induced HO-1 upregulation was significantly impaired in the lungs of 65-66-week-old mice than in 9-11-week-old mice at 2 and 24 h, although there were no differences in the magnitude of HO-1 upregulation in bronchiolar epithelium at 2 h. LPS-induced upregulation of HO-1 was observed in AMs from 22-week-old mice (1.8-fold), but not in AMs from 86-96-week-old mice in vitro. In summary, we demonstrated age-related defects in HO-1 induction in the whole lungs and in AMs in response to LPS.

KW - Acute lung injury

KW - Aging

KW - HO-1

KW - LPS

UR - http://www.scopus.com/inward/record.url?scp=61849126736&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=61849126736&partnerID=8YFLogxK

U2 - 10.1007/s10522-008-9164-4

DO - 10.1007/s10522-008-9164-4

M3 - Article

C2 - 18690550

AN - SCOPUS:61849126736

VL - 10

SP - 173

EP - 180

JO - Biogerontology

JF - Biogerontology

SN - 1389-5729

IS - 2

ER -