Evidence map›Paper›PMID 21930963›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

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

Shashi P Singh, Sravanthi Gundavarapu, Juan C Peña-Philippides, Jules Rir-Sima-ah, Neerad C Mishra, Julie A Wilder, Raymond J Langley, Kevin R Smith, Mohan L Sopori

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 93 citations in OpenAlex.

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  12. Experimental and therapeutic medicine · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Shashi P SinghRespiratory Immunology Division, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA.
Sravanthi Gundavarapu
Juan C Peña-Philippides
Jules Rir-Sima-ah
Neerad C Mishra
Julie A Wilder
Raymond J Langley
Kevin R Smith
Mohan L Sopori
Lovelace Respiratory Research Institute · US

Funding

DENDRITIC SIGNALING IN THE OLFACTORY BULBR01DC004208 · NIDCD · MONELL CHEMICAL SENSES CENTER · PI LOWE, GRAEME · 2001 to 2012
$2.9M
Nicotine &Immunopathogenesis of Cryptococcal meningitisR01DA017003 · NIDA · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI SOPORI, MOHAN L. · 2003 to 2007
$2.0M
T Cell Nicotinic ReceptorsR01DA004208 · NIDA · LOVELACE RESPIRATORY RESEARCH INSTITUTE · PI SOPORI, MOHAN L. · 1986 to 2003
$1.9M
NIDA NIH HHS R01 DA004208NIDA NIH HHS R01 DA017003NIDA NIH HHS R01 DA04208-17NIDCD NIH HHS R01 DC004208
6 · The paper itself

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.

Indexed as

AnimalsCell DifferentiationCell PolarityDown-RegulationFemaleGoblet CellsHumansMaleMiceMice, Inbred BALB CMucusPregnancyPrenatal Exposure Delayed EffectsRespiratory MucosaRisk FactorsTh2 CellsTobacco Smoke Pollution

Identifiers

PMID21930963
PMCPMC3197944
OpenAlexW2107007226

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.