Evidence map›Paper›PMID 19852193›Full record

ArticleAnnals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology2009

Decrease in airway mucous gene expression caused by treatment with anti-tumor necrosis factor alpha in a murine model of allergic asthma.

Paula J Busse, Teng Fei Zhang, Brian Schofield, Saikiran Kilaru, Sangita Patil, Xiu-Min Li

Abstract read
In one paragraph

Article in Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Anti-TNFα therapy in inflammatory lung diseases.Pharmacology & therapeutics · 2017
    Review
  5. Article
  6. Article
  7. Human neutrophil elastase-mediated goblet cell metaplasia is attenuated in TACE-deficient mice.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  8. The effect of oral tolerance on the allergic airway response in younger and aged mice.The Journal of asthma : official journal of the Association for the Care of Asthma · 2013
    Article
  9. Article
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

6 authors at 2 institutions in 1 country.

Paula J BusseDivision of Clinical Immunology, Mount Sinai School of Medicine, New York, New York 10029, USA. paula.busse@mssm.edu
Teng Fei Zhang
Brian Schofield
Saikiran Kilaru
Sangita Patil
Xiu-Min Li
Icahn School of Medicine at Mount Sinai · USJohns Hopkins University · US

Funding

Therapy (CHT) for AsthmaP01AT002647 · NCCIH · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI LI, XIU-MIN · 2005 to 2009
$5.8M
NCCIH NIH HHS P01 AT002647
6 · The paper itself

Abstract

backgroundMucous hypersecretion increases asthma morbidity and mortality. Tumor necrosis factor a (TNF-a) levels are elevated in bronchoalveolar fluid, sputum, and monocyte membranes in some patients with asthma. Anti-TNF-a decreased asthma exacerbations and improved forced expiratory volume in 1 second in these patients. Whether anti-TNF-a reduces mucous cell metaplasia or hyperplasia has not been evaluated.

objectiveTo investigate the role of anti-TNF-alpha in mucous hypersecretion.

methodsBALB/c mice sensitized intraperitoneally and challenged intratracheally with ovalbumin were treated with 250 microg of anti-TNF-alpha before ovalbumin sensitization and challenge or before only ovalbumin challenge. Control groups were sham treated. The tumor necrosis factor receptor (TNFR) mice (TNFR-/- and TNFR+/+) were identically sensitized and challenged. Seventy-two hours after the final challenge, the airway pressure time index (APTI), which measures airway hyperresponsiveness, was recorded. Mucous cell metaplasia was accessed by quantitative polymerase chain reaction for MUC-5AC (the epithelial cell mucous-inducing gene) and the percentage of periodic acid-Schiff (PAS) staining of bronchial epithelial cells. A human airway cell line (constitutively expressing MUC-5AC) was pretreated with a NF-kappaB inhibitor before TNF-alpha culture.

resultsThe mean (SE) fold change of MUC-5AC expression (compared with naive controls), the percentage of PAS-positive bronchiole epithelial cells, and the APTI decreased in BALB/c mice treated with anti-TNF-alpha before sensitization and challenge (4.9 [1.14], P = .007; 28.9% [6.8%], P < .001; and 545.8 [104.5] cm H2O/s, P < .001, respectively) and before challenge alone (9.3 [1.8], P = .03; 43.6% [10.7%], P = .009; and 896.8 [81.23] cm H2O/s, P = .06, respectively) compared with sham-treated mice (20.9 [3.9], 82.4% [1.8%], and 1,055 [30.6] cm H20/s, respectively). MUC-5AC expression decreased in ovalbumin sensitized or challenged TNFR-/- (2.41 [0.4]) compared with ovalbumin sensitized or challenged TNFR+/+ mice (18.4 [2.5], P < .001). TNF-alpha-induced MUC-5AC expression in human airway culture significantly decreased with pretreatment of a NF-kappaB inhibitor.

conclusionsAnti-TNF-alpha treatment reduces airway mucous cell metaplasia in a mouse model of asthma, which may in part underlie its beneficial effect as asthma therapy.

Indexed as

AnimalsAntibodies, MonoclonalAsthmaBronchoalveolar Lavage FluidCell LineFemaleGene ExpressionHistocytochemistryMiceMice, Inbred BALB CMice, KnockoutMucin 5ACOvalbuminReceptors, Tumor Necrosis FactorRespiratory MucosaReverse Transcriptase Polymerase Chain ReactionAntibodies, MonoclonalMucin 5ACOvalbuminReceptors, Tumor Necrosis FactorRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID19852193
PMCPMC4621000
OpenAlexW2151839659

What OpenQuestion holds

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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.