Evidence map›Paper›PMID 22578901›Full record

ArticleThe Journal of allergy and clinical immunology2012

Role of nicotinic receptors and acetylcholine in mucous cell metaplasia, hyperplasia, and airway mucus formation in vitro and in vivo.

Sravanthi Gundavarapu, Julie A Wilder, Neerad C Mishra, Jules Rir-Sima-Ah, Raymond J Langley, Shashi P Singh, Ali Imran Saeed, Richard J Jaramillo, Katherine M Gott, Juan Carlos Peña-Philippides and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
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  8. COVID-19 and COPD: a narrative review of the basic science and clinical outcomes.European respiratory review : an official journal of the European Respiratory Society · 2020
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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

14 authors at 4 institutions in 1 country.

Sravanthi GundavarapuLovelace Respiratory Research Institute, Albuquerque, NM 87108, USA. msopori@lrri.org
Julie A Wilder
Neerad C Mishra
Jules Rir-Sima-Ah
Raymond J Langley
Shashi P Singh
Ali Imran Saeed
Richard J Jaramillo
Katherine M Gott
Juan Carlos Peña-Philippides
Kevin S Harrod
J Michael McIntosh
Shilpa Buch
Mohan L Sopori
Lovelace Respiratory Research Institute · USUniversity of Nebraska Medical Center · USUniversity of New Mexico · USUniversity of Utah · US

Funding

Nicotine &Immunopathogenesis of Cryptococcal meningitisR01DA017003 · NIDA · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI SOPORI, MOHAN L. · 2003 to 2007
$2.0M
NIDA NIH HHS R01 DA017003NIDA NIH HHS R01-DA017003
6 · The paper itself

Abstract

backgroundAirway mucus hypersecretion is a key pathophysiologic feature in a number of lung diseases. Cigarette smoke/nicotine and allergens are strong stimulators of airway mucus; however, the mechanism of mucus modulation is unclear.

objectivesWe sought to characterize the pathway by which cigarette smoke/nicotine regulates airway mucus and identify agents that decrease airway mucus.

methodsIL-13 and γ-aminobutyric acid type A receptors (GABA(A)Rs) are implicated in airway mucus. We examined the role of IL-13 and GABA(A)Rs in nicotine-induced mucus formation in normal human bronchial epithelial (NHBE) and A549 cells and secondhand cigarette smoke-induced, ovalbumin-induced, or both mucus formation in vivo.

resultsNicotine promotes mucus formation in NHBE cells; however, the nicotine-induced mucus formation is independent of IL-13 but sensitive to the GABA(A)R antagonist picrotoxin. Airway epithelial cells express α7-, α9-, and α10-nicotinic acetylcholine receptors (nAChRs), and specific inhibition or knockdown of α7- but not α9/α10-nAChRs abrogates mucus formation in response to nicotine and IL-13. Moreover, addition of acetylcholine or inhibition of its degradation increases mucus in NHBE cells. Nicotinic but not muscarinic receptor antagonists block allergen- or nicotine/cigarette smoke-induced airway mucus formation in NHBE cells, murine airways, or both.

conclusionsNicotine-induced airway mucus formation is independent of IL-13, and α7-nAChRs are critical in airway mucous cell metaplasia/hyperplasia and mucus production in response to various promucoid agents, including IL-13. In the absence of nicotine, acetylcholine might be the biological ligand for α7-nAChRs to trigger airway mucus formation. α7-nAChRs are downstream of IL-13 but upstream of GABA(A)Rα2 in the MUC5AC pathway. Acetylcholine and α7-nAChRs might serve as therapeutic targets to control airway mucus.

Indexed as

Acetylcholinealpha7 Nicotinic Acetylcholine ReceptorBronchiEpithelial CellsHumansHyperplasiaInterleukin-13MetaplasiaMucusNicotineReceptors, GABA-AReceptors, NicotinicAcetylcholinealpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, humanInterleukin-13NicotineReceptors, GABA-AReceptors, Nicotinic

Identifiers

PMID22578901
PMCPMC3419772
OpenAlexW2091591049

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.