Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys

Lei Wang, Jesse P. Joad, Caiyun Zhong, Kent E Pinkerton

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Background: Exposure to environmental tobacco smoke (ETS) in early life has adverse effects on lung development and increases asthma incidence and susceptibility to infection. We have previously reported that perinatal and postnatal exposure to ETS in infant monkeys leads to an impaired TH1 immune response in peripheral blood. Objective: Determine whether ETS exposure during the perinatal period alters pulmonary immune maturation in the neonatal lung. Methods: Nonhuman primates were exposed to ETS from gestation day 50 to 13 months postnatal age (perinatal ETS) or from 6 to 13 months (postnatal ETS). Control animals were only exposed to filtered air. TH1 and TH2-related cytokines, chemokines, and their corresponding receptors as well as transcription factors were analyzed in lung tissues at 13 months. Results: Animals exposed to ETS beginning in utero exhibited more profound alterations in TH1 factors compared with animals exposed to ETS beginning at 6 months postnatal age. In perinatal ETS-exposed monkeys, mRNA for IFN-γ, IL-2, IFN-γ-inducible protein 10, monokine induced by IFN-γ, IFN-γ-inducible T-cell chemoattractant, CXC chemokine receptor 3, IL-12 bioactive p70 subunit, and T-bet were significantly downregulated, whereas in postnatal ETS-exposed monkeys, only IFN-γ, CXC chemokine receptor 3, and IL-12p70 were significantly downregulated. ETS effects on TH2 factors were less apparent and more variable: mRNA for thymus and activation-regulated chemokine was increased, and IL-10 protein was reduced. Conclusions: Environmental tobacco smoke exposure during early life enhances a local TH2 immunity by impairing normal pulmonary TH1 immune maturation. This effect was greater in animals beginning ETS exposure in utero.

Original languageEnglish (US)
JournalJournal of Allergy and Clinical Immunology
Volume122
Issue number2
DOIs
StatePublished - Aug 2008

Fingerprint

Smoke
Tobacco
Haplorhini
Lung
CXCR3 Receptors
Environmental Exposure
Down-Regulation
Chemokine CCL17
Monokines
Messenger RNA
Chemotactic Factors
Interleukin-12
Chemokines
Interleukin-10
Primates
Interleukin-2
Immunity
Proteins
Transcription Factors
Asthma

Keywords

  • Environmental tobacco smoke
  • lung development
  • T1 immune response

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys. / Wang, Lei; Joad, Jesse P.; Zhong, Caiyun; Pinkerton, Kent E.

In: Journal of Allergy and Clinical Immunology, Vol. 122, No. 2, 08.2008.

Research output: Contribution to journalArticle

@article{bd31038714a4404a845319a7c1cbc3ac,
title = "Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys",
abstract = "Background: Exposure to environmental tobacco smoke (ETS) in early life has adverse effects on lung development and increases asthma incidence and susceptibility to infection. We have previously reported that perinatal and postnatal exposure to ETS in infant monkeys leads to an impaired TH1 immune response in peripheral blood. Objective: Determine whether ETS exposure during the perinatal period alters pulmonary immune maturation in the neonatal lung. Methods: Nonhuman primates were exposed to ETS from gestation day 50 to 13 months postnatal age (perinatal ETS) or from 6 to 13 months (postnatal ETS). Control animals were only exposed to filtered air. TH1 and TH2-related cytokines, chemokines, and their corresponding receptors as well as transcription factors were analyzed in lung tissues at 13 months. Results: Animals exposed to ETS beginning in utero exhibited more profound alterations in TH1 factors compared with animals exposed to ETS beginning at 6 months postnatal age. In perinatal ETS-exposed monkeys, mRNA for IFN-γ, IL-2, IFN-γ-inducible protein 10, monokine induced by IFN-γ, IFN-γ-inducible T-cell chemoattractant, CXC chemokine receptor 3, IL-12 bioactive p70 subunit, and T-bet were significantly downregulated, whereas in postnatal ETS-exposed monkeys, only IFN-γ, CXC chemokine receptor 3, and IL-12p70 were significantly downregulated. ETS effects on TH2 factors were less apparent and more variable: mRNA for thymus and activation-regulated chemokine was increased, and IL-10 protein was reduced. Conclusions: Environmental tobacco smoke exposure during early life enhances a local TH2 immunity by impairing normal pulmonary TH1 immune maturation. This effect was greater in animals beginning ETS exposure in utero.",
keywords = "Environmental tobacco smoke, lung development, T1 immune response",
author = "Lei Wang and Joad, {Jesse P.} and Caiyun Zhong and Pinkerton, {Kent E}",
year = "2008",
month = "8",
doi = "10.1016/j.jaci.2008.04.011",
language = "English (US)",
volume = "122",
journal = "Journal of Allergy and Clinical Immunology",
issn = "0091-6749",
publisher = "Mosby Inc.",
number = "2",

}

TY - JOUR

T1 - Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys

AU - Wang, Lei

AU - Joad, Jesse P.

AU - Zhong, Caiyun

AU - Pinkerton, Kent E

PY - 2008/8

Y1 - 2008/8

N2 - Background: Exposure to environmental tobacco smoke (ETS) in early life has adverse effects on lung development and increases asthma incidence and susceptibility to infection. We have previously reported that perinatal and postnatal exposure to ETS in infant monkeys leads to an impaired TH1 immune response in peripheral blood. Objective: Determine whether ETS exposure during the perinatal period alters pulmonary immune maturation in the neonatal lung. Methods: Nonhuman primates were exposed to ETS from gestation day 50 to 13 months postnatal age (perinatal ETS) or from 6 to 13 months (postnatal ETS). Control animals were only exposed to filtered air. TH1 and TH2-related cytokines, chemokines, and their corresponding receptors as well as transcription factors were analyzed in lung tissues at 13 months. Results: Animals exposed to ETS beginning in utero exhibited more profound alterations in TH1 factors compared with animals exposed to ETS beginning at 6 months postnatal age. In perinatal ETS-exposed monkeys, mRNA for IFN-γ, IL-2, IFN-γ-inducible protein 10, monokine induced by IFN-γ, IFN-γ-inducible T-cell chemoattractant, CXC chemokine receptor 3, IL-12 bioactive p70 subunit, and T-bet were significantly downregulated, whereas in postnatal ETS-exposed monkeys, only IFN-γ, CXC chemokine receptor 3, and IL-12p70 were significantly downregulated. ETS effects on TH2 factors were less apparent and more variable: mRNA for thymus and activation-regulated chemokine was increased, and IL-10 protein was reduced. Conclusions: Environmental tobacco smoke exposure during early life enhances a local TH2 immunity by impairing normal pulmonary TH1 immune maturation. This effect was greater in animals beginning ETS exposure in utero.

AB - Background: Exposure to environmental tobacco smoke (ETS) in early life has adverse effects on lung development and increases asthma incidence and susceptibility to infection. We have previously reported that perinatal and postnatal exposure to ETS in infant monkeys leads to an impaired TH1 immune response in peripheral blood. Objective: Determine whether ETS exposure during the perinatal period alters pulmonary immune maturation in the neonatal lung. Methods: Nonhuman primates were exposed to ETS from gestation day 50 to 13 months postnatal age (perinatal ETS) or from 6 to 13 months (postnatal ETS). Control animals were only exposed to filtered air. TH1 and TH2-related cytokines, chemokines, and their corresponding receptors as well as transcription factors were analyzed in lung tissues at 13 months. Results: Animals exposed to ETS beginning in utero exhibited more profound alterations in TH1 factors compared with animals exposed to ETS beginning at 6 months postnatal age. In perinatal ETS-exposed monkeys, mRNA for IFN-γ, IL-2, IFN-γ-inducible protein 10, monokine induced by IFN-γ, IFN-γ-inducible T-cell chemoattractant, CXC chemokine receptor 3, IL-12 bioactive p70 subunit, and T-bet were significantly downregulated, whereas in postnatal ETS-exposed monkeys, only IFN-γ, CXC chemokine receptor 3, and IL-12p70 were significantly downregulated. ETS effects on TH2 factors were less apparent and more variable: mRNA for thymus and activation-regulated chemokine was increased, and IL-10 protein was reduced. Conclusions: Environmental tobacco smoke exposure during early life enhances a local TH2 immunity by impairing normal pulmonary TH1 immune maturation. This effect was greater in animals beginning ETS exposure in utero.

KW - Environmental tobacco smoke

KW - lung development

KW - T1 immune response

UR - http://www.scopus.com/inward/record.url?scp=48349139333&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=48349139333&partnerID=8YFLogxK

U2 - 10.1016/j.jaci.2008.04.011

DO - 10.1016/j.jaci.2008.04.011

M3 - Article

C2 - 18502491

AN - SCOPUS:48349139333

VL - 122

JO - Journal of Allergy and Clinical Immunology

JF - Journal of Allergy and Clinical Immunology

SN - 0091-6749

IS - 2

ER -