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Cited by 48Asthma and respiratory diseasesSmoking Behavior and CessationImmunotoxicology and immune responses

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

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Wang, Lei, Joad, Jesse P., Zhong, Caiyun, Pinkerton, Kent E.·2008·Journal of Allergy and Clinical Immunology
DOI 10.1016/j.jaci.2008.04.011
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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 T(H)1 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. T(H)1 and T(H)2-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 T(H)1 factors compared with animals exposed to ETS beginning at 6 months postnatal age. In perinatal ETS-exposed monkeys, mRNA for IFN-gamma, IL-2, IFN-gamma-inducible protein 10, monokine induced by IFN-gamma, IFN-gamma-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-gamma, CXC chemokine receptor 3, and IL-12p70 were significantly downregulated. ETS effects on T(H)2 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 T(H)2 immunity by impairing normal pulmonary T(H)1 immune maturation. This effect was greater in animals beginning ETS exposure in utero.

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  • In a primate model, in utero and postnatal smoke exposure decreased Th1 cytokine production, which correlated with decreased recruitment of Th1 immune cells to the lung parenchyma.

    “Similarly, in a primate model, Wang and colleagues 66 demonstrated decreased Th1 cytokine production after in utero and postnatal smoke exposure, which correlated with decreased recruitment of Th1 immune cells to the lung parenchyma.”

    From Impact of Tobacco Smoke and Nicotine Exposure on Lung Development (2016) · cites this paper as [66]

    The paper reports reduced Th1-associated cytokine expression after perinatal smoke exposure. But the section ‘ETS effects on the recruitment of CXCR3-bearing immune cells in the lung’ reports fewer CXCR3-positive cells in the subepithelium, not the lung parenchyma; it says alveolar-tissue counts did not differ significantly among groups. (LLM, conf=0.88)

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  • In infant monkeys exposed to in utero and early postnatal tobacco smoke, there was decreased expression of upstream and downstream interferon-g pathway genes that regulate interferon-g.

    “Wang and colleagues 66 examined the Th1 and Th2 pulmonary responses in lungs of infant monkeys exposed to in utero and early postnatal tobacco smoke”

    From Impact of Tobacco Smoke and Nicotine Exposure on Lung Development (2016) · cites this paper as [66]

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Research works printed but not linked: 4

  1. [30]30. Lu B, Humbles A, Bota D, Gerard C, Moser B, Soler D, et al. Structure and func- tion of the murine chemokine receptor CXCR3. Eur J Immunol 1999;29:3804-12.
  2. [35]35. O'Garra A. Commitment factors for T helper cells. Curr Biol 2000;10:R492-4.
  3. [54]54. Teague SV, Pinkerton KE, Goldsmith M, Gebremichael A, Chang S, Jenkins RA, et al. A sidestream cigarette smoke generation and exposure system for environ- mental tobacco smoke studies. Inhal Toxicol 1994;6:79-93.
  4. [55]55. Vogel CF, Zhao Y, Wong P, Young NF, Matsumura F. The use of c-src knockout mice for the identification of the main toxic signaling pathway of TCDD to induce wasting syndrome. J Biochem Mol Toxicol 2003;17:305-15.

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Authors
Wang, L., Joad, J. P., Zhong, C., & Pinkerton, K. E.
Affiliations
University of California, Davis (US)
Corresponding author
Pinkerton, Kent E.
ORCID
Venue
Journal of Allergy and Clinical Immunology
Publisher
Elsevier BV
Published
2008-08
Volume
122
Issue
2
Pages
400-406.e5
ISSN
0091-6749 (ISSN-L)
DOI
10.1016/j.jaci.2008.04.011
OpenAlex
W2115736597
Cited by
48
References
55
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2022: 2 · 2021: 2 · 2020: 1 · 2018: 1 · 2017: 5 · 2016: 2 · 2015: 7 · 2014: 5 · 2013: 3 · 2012: 3
FWCI
3.12
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Allergy and Clinical Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (ES-05707, RR00169)
  • National Institute of Environmental Health Sciences (R01ES011634, ES05707)
  • National Center for Research Resources (P51RR000169)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords
environmental tobacco smoke, Th1 response, Th2 immune response, cytokines, chemokines, interferon-gamma, IL-12p70, CCR3, T-bet, IL-10, neonatal lung, non-human primates, asthma susceptibility
MeSH terms
Animals, Female, Lung, Macaca mulatta, RNA, Messenger, Tobacco Smoke Pollution, Transcription Factors, Down-Regulation, Cytokines, Interleukin-10, Th1 Cells, Th2 Cells, Interleukin-12, Maternal Exposure, Receptors, CXCR3

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