Early life exposure to environmental tobacco smoke alters immune response to asbestos via a shift in inflammatory phenotype resulting in increased disease development

Traci Ann Brown, Andrij Holian, Kent E Pinkerton, Joong Won Lee, Yoon Hee Cho

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Asbestos in combination with tobacco smoke exposure reportedly leads to more severe physiological consequences than asbestos alone; limited data also show an increased disease risk due to environmental tobacco smoke (ETS) exposure. Environmental influences during gestation and early lung development can result in physiological changes that alter risk for disease development throughout an individual’s lifetime. Therefore, maternal lifestyle may impact the ability of offspring to subsequently respond to environmental insults and alter overall disease susceptibility. In this study, we examined the effects of exposure to ETS in utero and during early postnatal development on asbestos-related inflammation and disease in adulthood. ETS exposure in utero appeared to shift inflammation towards a Th2 phenotype, via suppression of Th1 inflammatory cytokine production. This effect was further pronounced in mice exposed to ETS in utero and during early postnatal development. In utero ETS exposure led to increased collagen deposition, a marker of fibrotic disease, when the offspring was later exposed to asbestos, which was further increased with additional ETS exposure during early postnatal development. These data suggest that ETS exposure in utero alters the immune responses and leads to greater disease development after asbestos exposure, which is further exacerbated when exposure to ETS continues during early postnatal development.

Original languageEnglish (US)
Pages (from-to)349-356
Number of pages8
JournalInhalation Toxicology
Volume28
Issue number8
DOIs
StatePublished - Jul 2 2016

Fingerprint

Tobacco
Asbestos
Environmental Exposure
Smoke
Phenotype
Inflammation
Aptitude
Disease Susceptibility
Life Style
Collagen
Mothers
Cytokines
Pregnancy
Lung

Keywords

  • Asbestos
  • environmental tobacco smoke
  • fibrosis
  • inflammation

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Early life exposure to environmental tobacco smoke alters immune response to asbestos via a shift in inflammatory phenotype resulting in increased disease development. / Brown, Traci Ann; Holian, Andrij; Pinkerton, Kent E; Lee, Joong Won; Cho, Yoon Hee.

In: Inhalation Toxicology, Vol. 28, No. 8, 02.07.2016, p. 349-356.

Research output: Contribution to journalArticle

@article{b99b74e8266a4c9fa00a0cf53c40f443,
title = "Early life exposure to environmental tobacco smoke alters immune response to asbestos via a shift in inflammatory phenotype resulting in increased disease development",
abstract = "Asbestos in combination with tobacco smoke exposure reportedly leads to more severe physiological consequences than asbestos alone; limited data also show an increased disease risk due to environmental tobacco smoke (ETS) exposure. Environmental influences during gestation and early lung development can result in physiological changes that alter risk for disease development throughout an individual’s lifetime. Therefore, maternal lifestyle may impact the ability of offspring to subsequently respond to environmental insults and alter overall disease susceptibility. In this study, we examined the effects of exposure to ETS in utero and during early postnatal development on asbestos-related inflammation and disease in adulthood. ETS exposure in utero appeared to shift inflammation towards a Th2 phenotype, via suppression of Th1 inflammatory cytokine production. This effect was further pronounced in mice exposed to ETS in utero and during early postnatal development. In utero ETS exposure led to increased collagen deposition, a marker of fibrotic disease, when the offspring was later exposed to asbestos, which was further increased with additional ETS exposure during early postnatal development. These data suggest that ETS exposure in utero alters the immune responses and leads to greater disease development after asbestos exposure, which is further exacerbated when exposure to ETS continues during early postnatal development.",
keywords = "Asbestos, environmental tobacco smoke, fibrosis, inflammation",
author = "Brown, {Traci Ann} and Andrij Holian and Pinkerton, {Kent E} and Lee, {Joong Won} and Cho, {Yoon Hee}",
year = "2016",
month = "7",
day = "2",
doi = "10.1080/08958378.2016.1175526",
language = "English (US)",
volume = "28",
pages = "349--356",
journal = "Inhalation Toxicology",
issn = "0895-8378",
publisher = "Informa Healthcare",
number = "8",

}

TY - JOUR

T1 - Early life exposure to environmental tobacco smoke alters immune response to asbestos via a shift in inflammatory phenotype resulting in increased disease development

AU - Brown, Traci Ann

AU - Holian, Andrij

AU - Pinkerton, Kent E

AU - Lee, Joong Won

AU - Cho, Yoon Hee

PY - 2016/7/2

Y1 - 2016/7/2

N2 - Asbestos in combination with tobacco smoke exposure reportedly leads to more severe physiological consequences than asbestos alone; limited data also show an increased disease risk due to environmental tobacco smoke (ETS) exposure. Environmental influences during gestation and early lung development can result in physiological changes that alter risk for disease development throughout an individual’s lifetime. Therefore, maternal lifestyle may impact the ability of offspring to subsequently respond to environmental insults and alter overall disease susceptibility. In this study, we examined the effects of exposure to ETS in utero and during early postnatal development on asbestos-related inflammation and disease in adulthood. ETS exposure in utero appeared to shift inflammation towards a Th2 phenotype, via suppression of Th1 inflammatory cytokine production. This effect was further pronounced in mice exposed to ETS in utero and during early postnatal development. In utero ETS exposure led to increased collagen deposition, a marker of fibrotic disease, when the offspring was later exposed to asbestos, which was further increased with additional ETS exposure during early postnatal development. These data suggest that ETS exposure in utero alters the immune responses and leads to greater disease development after asbestos exposure, which is further exacerbated when exposure to ETS continues during early postnatal development.

AB - Asbestos in combination with tobacco smoke exposure reportedly leads to more severe physiological consequences than asbestos alone; limited data also show an increased disease risk due to environmental tobacco smoke (ETS) exposure. Environmental influences during gestation and early lung development can result in physiological changes that alter risk for disease development throughout an individual’s lifetime. Therefore, maternal lifestyle may impact the ability of offspring to subsequently respond to environmental insults and alter overall disease susceptibility. In this study, we examined the effects of exposure to ETS in utero and during early postnatal development on asbestos-related inflammation and disease in adulthood. ETS exposure in utero appeared to shift inflammation towards a Th2 phenotype, via suppression of Th1 inflammatory cytokine production. This effect was further pronounced in mice exposed to ETS in utero and during early postnatal development. In utero ETS exposure led to increased collagen deposition, a marker of fibrotic disease, when the offspring was later exposed to asbestos, which was further increased with additional ETS exposure during early postnatal development. These data suggest that ETS exposure in utero alters the immune responses and leads to greater disease development after asbestos exposure, which is further exacerbated when exposure to ETS continues during early postnatal development.

KW - Asbestos

KW - environmental tobacco smoke

KW - fibrosis

KW - inflammation

UR - http://www.scopus.com/inward/record.url?scp=84965046255&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84965046255&partnerID=8YFLogxK

U2 - 10.1080/08958378.2016.1175526

DO - 10.1080/08958378.2016.1175526

M3 - Article

C2 - 27138493

AN - SCOPUS:84965046255

VL - 28

SP - 349

EP - 356

JO - Inhalation Toxicology

JF - Inhalation Toxicology

SN - 0895-8378

IS - 8

ER -