Evidence map›Paper›PMID 22773729›Full record

ArticleAmerican journal of respiratory and critical care medicine2012

Alveolar macrophages from overweight/obese subjects with asthma demonstrate a proinflammatory phenotype.

Njira L Lugogo, John W Hollingsworth, Druhan L Howell, Loretta G Que, Dave Francisco, Tony D Church, Erin N Potts-Kant, Jennifer L Ingram, Ying Wang, Sin-Ho Jung and 1 more

Retracted Registry-linked trialAbstract readRetracted Publication
In one paragraph

Article in American journal of respiratory and critical care medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. It is linked to trial NCT02975258 (Adiposity and Airway Inflammation in HIV-Associated Airway Disease), which is not on this map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.5field-weighted citation impact, top 3% 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.

NCT02975258 completednot on this mapstarted 2015, after this paper: background citation

Adiposity and Airway Inflammation in HIV-Associated Airway Disease

TypeobservationalSponsorUniversity of PittsburghRan2015 to 2017Enrolled102ConditionsAsthma, HIV, AdiposityArmsBlood draw, Questionnaires, Spirometry, Methacholine challenge test, Quantitative CT scans
3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 71 citations in OpenAlex.

  1. Comorbidities of sarcoidosis.Annals of medicine · 2022
    Review
  2. Article
  3. Epidemiology of sarcoidosis: current findings and future directions.Therapeutic advances in chronic disease · 2018
    Review
  4. Late-onset asthma: current perspectives.Journal of asthma and allergy · 2018
    Review
  5. Article
  6. Article
  7. Article
  8. The impact of diet on asthma and allergic diseases.Nature reviews. Immunology · 2015
    Review
  9. Article
  10. Article
  11. Review
  12. Emerging molecular phenotypes of asthma.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Is there a link between obesity and asthma?Allergy, asthma & immunology research · 2014
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Njira L LugogoDuke University Medical Center, P.O. Box 2629, Durham, NC 27710, USA. njira.lugogo@duke.edu
John W Hollingsworth
Druhan L Howell
Loretta G Que
Dave Francisco
Tony D Church
Erin N Potts-Kant
Jennifer L Ingram
Ying Wang
Sin-Ho Jung
Monica Kraft
Duke Medical Center · USDuke University · USUniversity of South Alabama · US

Funding

MATRIX REGULATION OF FIBROPROLIFERATIVE LUNG DISEASEP50HL084917 · NHLBI · DUKE UNIVERSITY · PI ROCKMAN, HOWARD A · 2006 to 2010
$13.2M
Surfactant Protein-A Regulation of Innate Immunityin AsthmaP01AI081672 · NIAID · DUKE UNIVERSITY · PI SUNDY, JOHN S · 2009 to 2013
$7.4M
OZONE PRIMES PULMONARY INNATE IMMUNITYR01ES016126 · NIEHS · OHIO STATE UNIVERSITY · PI HOLLINGSWORTH, JOHN W · 2008 to 2012
$2.3M
GSNO Reductase, S-Nitrosothiols, and AsthmaR01HL086887 · NHLBI · DUKE UNIVERSITY · PI QUE, LORETTA G · 2007 to 2011
$1.8M
INCREASED ENDOTHELIN VASOCONSTRICTOR ACTIVITY IN ESSENTIAL HYPERTENSIONZ01HL005009 · NHLBI · HEART, LUNG, AND BLOOD INSTITUTE · PI PANZA, J A · 1997 to 1998
–
NHLBI NIH HHS HL-05-009NHLBI NIH HHS HL086887NHLBI NIH HHS P50 HL084917NHLBI NIH HHS P50-HL-084917NHLBI NIH HHS R01 HL086887NIAID NIH HHS AI081672NIAID NIH HHS P01 AI081672NIEHS NIH HHS ES016126NIEHS NIH HHS R01 ES016126
6 · The paper itself

Abstract

rationaleObesity is associated with increased prevalence and severity of asthma. Adipose tissue macrophages can contribute to the systemic proinflammatory state associated with obesity. However, it remains unknown whether alveolar macrophages have a unique phenotype in overweight/obese patients with asthma.

objectivesWe hypothesized that leptin levels would be increased in the bronchoalveolar lavage fluid from overweight/obese subjects and, furthermore, that leptin would alter the response of alveolar macrophages to bacterial LPS.

methodsForty-two subjects with asthma and 46 healthy control subjects underwent research bronchoscopy. Bronchoalveolar lavage fluid from 66 was analyzed for the level of cellular inflammation, cytokines, and soluble leptin. Cultured primary macrophages from 22 subjects were exposed to LPS, leptin, or leptin plus LPS. Cytokines were measured in the supernatants. MEASUREMENTS AND MAIN

resultsLeptin levels were increased in overweight/obese subjects, regardless of asthma status (P = 0.013), but were significantly higher in overweight/obese subjects with asthma. Observed levels of tumor necrosis factor-α were highest in overweight/obese subjects with asthma. Ex vivo studies of primary alveolar macrophages indicated that the response to LPS was most robust in alveolar macrophages from overweight/obese subjects with asthma and that preexposure to high-dose leptin enhanced the proinflammatory response. Leptin alone was sufficient to induce production of proinflammatory cytokines from macrophages derived from overweight/obese subjects with asthma.

conclusionsEx vivo studies indicate that alveolar macrophages derived from overweight/obese subjects with asthma are uniquely sensitive to leptin. This macrophage phenotype, in the context of higher levels of soluble leptin, may contribute to the pathogenesis of airway disease associated with obesity.

Indexed as

AdolescentAdultAgedAnalysis of VarianceAsthmaBiomarkersBronchoalveolar Lavage FluidBronchoscopyCase-Control StudiesCells, CulturedCytokinesEnzyme-Linked Immunosorbent AssayFemaleHumansLeptinLinear ModelsBiomarkersCytokinesLeptinlipopolysaccharide, Escherichia coli O111 B4Lipopolysaccharides

Identifiers

PMID22773729
PMCPMC3443798
OpenAlexW2098926324

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.