Cited by 93Asthma and respiratory diseasesSmoking Behavior and CessationChronic Obstructive Pulmonary Disease (COPD) Research

Prenatal secondhand cigarette smoke promotes Th2 polarization and impairs goblet cell differentiation and airway mucus formation

Open access
Singh, Shashi P, Gundavarapu, Sravanthi, Peña-Philippides, Juan C, Rir-sima-ah, Jules, Mishra, Neerad C, Wilder, Julie A, Langley, Raymond J, Smith, Kevin R +1 more·2011·The Journal of Immunology

Abstract

Parental, particularly maternal, smoking increases the risk for childhood allergic asthma and infection. Similarly, in a murine allergic asthma model, prenatal plus early postnatal exposure to secondhand cigarette smoke (SS) exacerbates airways hyperreactivity and Th2 responses in the lung. However, the mechanism and contribution of prenatal versus early postnatal SS exposure on allergic asthma remain unresolved. To identify the effects of prenatal and/or early postnatal SS on allergic asthma, BALB/c dams and their offspring were exposed gestationally and/or 8–10 wk postbirth to filtered air or SS. Prenatal, but not postnatal, SS strongly increased methacholine and allergen (Aspergillus)-induced airway resistance, Th2 cytokine levels, and atopy and activated the Th2-polarizing pathway GATA3/Lck/ERK1/2/STAT6. Either prenatal and/or early postnatal SS downregulated the Th1-specific transcription factor T-bet and, surprisingly, despite high levels of IL-4/IL-13, dramatically blocked the allergen-induced mucous cell metaplasia, airway mucus formation, and the expression of mucus-related genes/proteins: Muc5ac, γ-aminobutyric acid A receptors, and SAM pointed domain-containing Ets-like factor. Given that SS/nicotine exposure of normal adult mice promotes mucus formation, the results suggested that fetal and neonatal lung are highly sensitive to cigarette smoke. Thus, although the gestational SS promotes Th2 polarization/allergic asthma, it may also impair and/or delay the development of fetal and neonatal lung, affecting mucociliary clearance and Th1 responses. Together, this may explain the increased susceptibility of children from smoking parents to allergic asthma and childhood respiratory infections.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.4049/jimmunol.1101567

Cites

76 of 76 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In animal models, exposure to in utero and early postnatal tobacco smoke is associated with a Th1 and Th2 imbalance and increased susceptibility to lower respiratory tract infections.

    “In animal models, exposure to in utero and early postnatal tobacco smoke has been associated with a Th1 and Th2 imbalance and increased susceptibility to lower respiratory tract infections.31”
  • In animal models, exposure to in utero and early postnatal tobacco smoke is associated with a Th1 and Th2 imbalance and an increased susceptibility to airway reactivity.

    “In animal models, exposure to in utero and early postnatal tobacco smoke has been associated with a Th1 and Th2 imbalance and an increased susceptibility to airway reactivity.31”
  • Prenatal smoke exposure caused Th1 and Th2 changes in mice after Aspergillus sensitization.

    “| Y Interferon-g | Prenatal smoke exposure caused Th1 and Th2 changes in | 31 |”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Singh, S. P., Gundavarapu, S., Peña-Philippides, J. C., Rir-sima-ah, J., Mishra, N. C., Wilder, J. A., Langley, R. J., Smith, K. R., & Sopori, M. L.
Affiliations
  • Respiratory Immunology Division, Lovelace Respiratory Research Institute , Albuquerque, NM 87108
  • Lovelace Respiratory Research Institute (US)
Corresponding author
Gundavarapu, Sravanthi
Venue
The Journal of Immunology
Published
2011-11-01
Volume
187
Issue
9
Pages
4542-4552
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W2107007226
Cited by
93
References
76
Citations by year
2026: 2 · 2025: 2 · 2024: 3 · 2023: 2 · 2022: 7 · 2021: 6 · 2020: 11 · 2019: 6 · 2018: 7 · 2017: 11 · 2016: 5 · 2015: 8 · 2014: 7 · 2013: 12 · 2012: 3
FWCI
5.02
Type
journal article
Language
en
Open access
Locations
  • The Journal of Immunology (publishedVersion, public-domain)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute on Drug Abuse (R01DA017003, R01 DA04208-17, R01DA004208)
  • National Institute on Deafness and Other Communication Disorders (R01DC004208)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
Keywords
allergic asthma, Th2 polarization, goblet cell differentiation, mucous cell metaplasia, STAT6 signaling, GATA3, T-bet, IL-4/IL-13, fetal lung development, neonatal lung, airway hyperresponsiveness, maternal smoking, mucociliary clearance
MeSH terms
Animals, Cell Differentiation, Female, Humans, Male, Mice, Inbred BALB C, Mucus, Pregnancy, Prenatal Exposure Delayed Effects, Risk Factors, Tobacco Smoke Pollution, Down-Regulation, Up-Regulation, Cell Polarity, Th2 Cells, Goblet Cells, Respiratory Mucosa, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review