Evidence map›Paper›PMID 36732772›Full record

ArticleRespiratory research2023

Lung Inflammation in alpha-1-antitrypsin deficient individuals with normal lung function.

Nurdan Kokturk, Nazli Khodayari, Jorge Lascano, E Leonard Riley, Mark L Brantly

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.2field-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.

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

22 citing papers in PubMed, 30 citations in OpenAlex.

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  15. [Alpha 1-antitrypsin deficiency].Innere Medizin (Heidelberg, Germany) · 2024
    Review
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  17. Review
  18. Heterogeneity in Neutrophil Extracellular Traps from Healthy Human Subjects.International journal of molecular sciences · 2023
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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

5 authors at 3 institutions in 2 countries.

Nurdan KokturkDivision of Pulmonary, Critical Care and Sleep Medicine, J. Hillis Miller Health Science Center, University of Florida College of Medicine, P.O. Box 100225, Gainesville, FL, 32610-0225, USA.
Nazli KhodayariDivision of Pulmonary, Critical Care and Sleep Medicine, J. Hillis Miller Health Science Center, University of Florida College of Medicine, P.O. Box 100225, Gainesville, FL, 32610-0225, USA.
Jorge LascanoDivision of Pulmonary, Critical Care and Sleep Medicine, J. Hillis Miller Health Science Center, University of Florida College of Medicine, P.O. Box 100225, Gainesville, FL, 32610-0225, USA.
E Leonard RileyKansas City Veterans Affair Medical Center, Kansas, TX, USA.
Mark L BrantlyDivision of Pulmonary, Critical Care and Sleep Medicine, J. Hillis Miller Health Science Center, University of Florida College of Medicine, P.O. Box 100225, Gainesville, FL, 32610-0225, USA. mbrantly@ufl.edu.
Florida College · USKansas City VA Medical Center · USUniversity of Florida Health Science Center · US

Funding

Anti-Inflammatory Role of Alpha-1 Antitrypsin in LungK24HL004456 · NHLBI · UNIVERSITY OF FLORIDA · PI BRANTLY, MARK LOUIS · 2002 to 2006
$670k
MOLECULAR CHARACTERISTICS AND CLINICAL ASPECTS OF ALPHA 1-ANTITRYPSIN DEFICIENCYZ01HL002538 · NHLBI · HEART, LUNG, AND BLOOD INSTITUTE · PI MOSS, J · 1995 to 1998
–
Intramural NIH HHS Z01 HL002538NHLBI NIH HHS K24 HL004456
6 · The paper itself

Abstract

backgroundAlpha-1-antitrypsin deficient (AATD) individuals are prone to develop early age of onset chronic obstructive pulmonary disease (COPD) more severe than non-genetic COPD. Here, we investigated the characteristics of lower respiratory tract of AATD individuals prior to the onset of clinically significant COPD.

methodsBronchoalveolar lavage was performed on 22 AATD with normal lung function and 14 healthy individuals. Cell counts and concentrations of proteases, alpha-1-antitrypsin and proinflammatory mediators were determined in the bronchoalveolar lavage fluid from study subjects. In order to determine the airway inflammation, we also analyzed immune cell components of the large airways from bronchial biopsies using immunohistochemistry in both study subjects. Finally, we made comparisons between airway inflammation and lung function rate of decline using four repeated lung function tests over one year in AATD individuals.

resultsAATD individuals with normal lung function had 3 folds higher neutrophil counts, 2 folds increase in the proteases levels, and 2-4 folds higher levels of IL-8, IL-6, IL-1β, and leukotriene B4 in their epithelial lining fluid compared to controls. Neutrophil elastase levels showed a positive correlation with the levels of IL-8 and neutrophils in AATD epithelial lining fluid. AATD individuals also showed a negative correlation of baseline FEV

conclusionMild inflammation is present in the lower respiratory tract and airways of AATD individuals despite having normal lung function. A declining trend was also noticed in the lung function of AATD individuals which was correlated with pro-inflammatory phenotype of their lower respiratory tract. This results suggest the presence of proinflammatory phenotype in AATD lungs. Therefore, early anti-inflammatory therapies may be a potential strategy to prevent progression of lung disease in AATD individuals.

Indexed as

alpha 1-Antitrypsin DeficiencyPneumoniaPulmonary Disease, Chronic Obstructivealpha 1-AntitrypsinHumansInflammationInterleukin-8Leukocyte ElastaseLungalpha 1-AntitrypsinInterleukin-8Leukocyte ElastaseEpithelial lining fluidNeutrophil elastaseProtease inhibitorPulmonary function

Identifiers

PMID36732772
PMCPMC9893669
OpenAlexW4318983123

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.