Evidence map›Paper›PMID 25957290›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

Alterations of lung microbiota in a mouse model of LPS-induced lung injury.

Valeriy Poroyko, Fanyong Meng, Angelo Meliton, Taras Afonyushkin, Alexander Ulanov, Ekaterina Semenyuk, Omar Latif, Vera Tesic, Anna A Birukova, Konstantin G Birukov

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 102 citations in OpenAlex.

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  17. Frontiers in cellular and infection microbiology · 2023
    Article
  18. Exposure to particulate matter 2.5 leading to lung microbiome disorder and the alleviation effect ofInternational journal of occupational medicine and environmental health · 2022
    Article
  19. Observational
  20. Acute Endotoxemia-Induced Respiratory and Intestinal Dysbiosis.International journal of molecular sciences · 2022
    Article

2 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Valeriy PoroykoDepartment of Pediatrics, The University of Chicago, Chicago, Illinois; poroyko@uchicago.edu.
Fanyong MengSection of Pulmonary and Critical Medicine, Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, Illinois;
Angelo MelitonSection of Pulmonary and Critical Medicine, Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, Illinois;
Taras AfonyushkinSection of Pulmonary and Critical Medicine, Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, Illinois;
Alexander UlanovRoy J. Carver Biotechnology Center, University of Illinois at Urbana-Champaign;
Ekaterina SemenyukDepartment of Microbiology and Immunology, Loyola University Chicago, Stritch School of Medicine, Maywood, Illinois;
Omar LatifDepartment of Medicine, The University of Chicago, Chicago, Illinois; and.
Vera TesicDepartment of Pathology, University of Chicago, Chicago, Illinois.
Anna A BirukovaSection of Pulmonary and Critical Medicine, Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, Illinois;
Konstantin G BirukovSection of Pulmonary and Critical Medicine, Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, Illinois;
University of Chicago · USLoyola University Chicago · USUniversity of Illinois Urbana-Champaign · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Control of Lung Permeability by Oxidized PhospholipidsR01HL076259 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2004 to 2023
$6.8M
Molecular control of lung endothelial barrier function in ALIR01HL087823 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2008 to 2020
$4.6M
Microtubule-associated regulation of acute lung injuryR01HL107920 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOVA, ANNA · 2011 to 2019
$2.8M
Interplay of diet and the metabolome in establishment of the juvenile gut microbiR21AI099713 · NIAID · UNIVERSITY OF CHICAGO · PI ALVERDY, JOHN C · 2012 to 2013
$448k
Microtubule-associated regulation of acute lung injuryR56HL107920 · NHLBI · UNIVERSITY OF CHICAGO · PI BIRUKOVA, ANNA · 2015 to 2015
$395k
NCATS NIH HHS UL1 TR000430NHLBI NIH HHS HL087823NHLBI NIH HHS HL107920NHLBI NIH HHS R01 HL076259NHLBI NIH HHS R01 HL087823NHLBI NIH HHS R01 HL107920NHLBI NIH HHS R56 HL107920NIAID NIH HHS 1R21AI099713-01NIAID NIH HHS R21 AI099713
6 · The paper itself

Abstract

Acute lung injury (ALI) and the more severe acute respiratory distress syndrome are common responses to a variety of infectious and noninfectious insults. We used a mouse model of ALI induced by intratracheal administration of sterile bacterial wall lipopolysaccharide (LPS) to investigate the changes in innate lung microbiota and study microbial community reaction to lung inflammation and barrier dysfunction induced by endotoxin insult. One group of C57BL/6J mice received LPS via intratracheal injection (n = 6), and another received sterile water (n = 7). Bronchoalveolar lavage (BAL) was performed at 72 h after treatment. Bacterial DNA was extracted and used for qPCR and 16S rRNA gene-tag (V3-V4) sequencing (Illumina). The bacterial load in BAL from ALI mice was increased fivefold (P = 0.03). The community complexity remained unchanged (Simpson index, P = 0.7); the Shannon diversity index indicated the increase of community evenness in response to ALI (P = 0.07). Principal coordinate analysis and analysis of similarity (ANOSIM) test (P = 0.005) revealed a significant difference between microbiota of control and ALI groups. Bacteria from families Xanthomonadaceae and Brucellaceae increased their abundance in the ALI group as determined by Metastats test (P < 0.02). In concordance with the 16s-tag data, Stenotrohomonas maltophilia (Xanthomonadaceae) and Ochrobactrum anthropi (Brucellaceae) were isolated from lungs of mice from both groups. Metabolic profiling of BAL detected the presence of bacterial substrates suitable for both isolates. Additionally, microbiota from LPS-treated mice intensified IL-6-induced lung inflammation in naive mice. We conclude that the morbid transformation of ALI microbiota was attributed to the set of inborn opportunistic pathogens thriving in the environment of inflamed lung, rather than the external infectious agents.

Indexed as

AnimalsBase SequenceBronchoalveolar Lavage FluidBrucellaceaeDisease Models, AnimalDNA, BacterialLipopolysaccharidesLungLung InjuryMiceMice, Inbred C57BLMicrobiotaRespiratory Distress SyndromeRNA, Ribosomal, 16SSequence Analysis, DNAXanthomonadaceaeDNA, BacterialLipopolysaccharidesRNA, Ribosomal, 16Sacute lung injuryLPSmetabolic profilingmicrobiota

Identifiers

PMID25957290
PMCPMC4491514
OpenAlexW2271412575

What OpenQuestion holds

Textmetadata
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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.