Unique patterns of lower respiratory tract microbiota are associated with inflammation and hospital mortality in acute respiratory distress syndrome.
Aged
Aged, 80 and over
Angiopoietin-2
/ analysis
Bronchoalveolar Lavage Fluid
/ chemistry
Case-Control Studies
Female
Hospital Mortality
Humans
Interleukin-6
/ analysis
Interleukin-8
/ analysis
Lung
/ metabolism
Male
Middle Aged
Pneumonia
/ blood
Prognosis
Receptor for Advanced Glycation End Products
/ analysis
Respiratory Distress Syndrome
/ blood
Respiratory Tract Infections
/ blood
Risk Assessment
Risk Factors
16S rRNA
Acute respiratory distress syndrome
Bronchoalveolar lavage
Lung
Pneumonia
Sepsis
Journal
Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633
Informations de publication
Date de publication:
06 Nov 2019
06 Nov 2019
Historique:
received:
22
07
2019
accepted:
30
09
2019
entrez:
8
11
2019
pubmed:
7
11
2019
medline:
28
4
2020
Statut:
epublish
Résumé
The lung microbiome maintains the homeostasis of the immune system within the lungs. In acute respiratory distress syndrome (ARDS), the lung microbiome is enriched with gut-derived bacteria; however, the specific microbiome associated with morbidity and mortality in patients with ARDS remains unclear. This study investigated the specific patterns of the lung microbiome that are correlated with mortality in ARDS patients. We analyzed the lung microbiome from the bronchoalveolar lavage fluid (BALF) of patients with ARDS and control subjects. We measured the copy numbers of 16S rRNA and the serum and BALF cytokines (interleukin [IL]-6, IL-8, receptor for advanced glycation end products, and angiopoietin-2). We analyzed 47 mechanically ventilated patients diagnosed with (n = 40) or without (n = 7; control) ARDS. The alpha diversity was significantly decreased in ARDS patients compared with that of the controls (6.24 vs. 8.07, P = 0.03). The 16S rRNA gene copy numbers tended to be increased in the ARDS group compared with the controls (3.83 × 10 The lung bacterial burden tended to be increased, and the alpha diversity was significantly decreased in ARDS patients. The decreased Betaproteobacteria and increased Staphylococcus, Streptococcus and Enterobacteriaceae might represent a unique microbial community structure correlated with increased serum IL-6 and hospital mortality. The institutional review boards of Hiroshima University (Trial registration: E-447-4, registered 16 October 2019) and Kyoto Prefectural University of Medicine (Trial registration: ERB-C-973, registered 19 October 2017) approved an opt-out method of informed consent.
Sections du résumé
BACKGROUND
BACKGROUND
The lung microbiome maintains the homeostasis of the immune system within the lungs. In acute respiratory distress syndrome (ARDS), the lung microbiome is enriched with gut-derived bacteria; however, the specific microbiome associated with morbidity and mortality in patients with ARDS remains unclear. This study investigated the specific patterns of the lung microbiome that are correlated with mortality in ARDS patients.
METHODS
METHODS
We analyzed the lung microbiome from the bronchoalveolar lavage fluid (BALF) of patients with ARDS and control subjects. We measured the copy numbers of 16S rRNA and the serum and BALF cytokines (interleukin [IL]-6, IL-8, receptor for advanced glycation end products, and angiopoietin-2).
RESULTS
RESULTS
We analyzed 47 mechanically ventilated patients diagnosed with (n = 40) or without (n = 7; control) ARDS. The alpha diversity was significantly decreased in ARDS patients compared with that of the controls (6.24 vs. 8.07, P = 0.03). The 16S rRNA gene copy numbers tended to be increased in the ARDS group compared with the controls (3.83 × 10
CONCLUSIONS
CONCLUSIONS
The lung bacterial burden tended to be increased, and the alpha diversity was significantly decreased in ARDS patients. The decreased Betaproteobacteria and increased Staphylococcus, Streptococcus and Enterobacteriaceae might represent a unique microbial community structure correlated with increased serum IL-6 and hospital mortality.
TRIAL REGISTRATION
BACKGROUND
The institutional review boards of Hiroshima University (Trial registration: E-447-4, registered 16 October 2019) and Kyoto Prefectural University of Medicine (Trial registration: ERB-C-973, registered 19 October 2017) approved an opt-out method of informed consent.
Identifiants
pubmed: 31694652
doi: 10.1186/s12931-019-1203-y
pii: 10.1186/s12931-019-1203-y
pmc: PMC6836399
doi:
Substances chimiques
AGER protein, human
0
ANGPT2 protein, human
0
Angiopoietin-2
0
CXCL8 protein, human
0
IL6 protein, human
0
Interleukin-6
0
Interleukin-8
0
Receptor for Advanced Glycation End Products
0
Types de publication
Journal Article
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
246Subventions
Organisme : Japan Society for the Promotion of Science
ID : 18K16518
Organisme : Japan Society for the Promotion of Science
ID : 18K16184
Organisme : Japan Society for the Promotion of Science
ID : 18H03040
Organisme : Japan Society for the Promotion of Science
ID : 17K17053
Références
Nat Microbiol. 2016 Jul 18;1(10):16113
pubmed: 27670109
Thorax. 2013 Dec;68(12):1150-6
pubmed: 23945167
Am J Respir Crit Care Med. 2016 Nov 15;194(10):1252-1263
pubmed: 27248293
J Allergy Clin Immunol. 2013 Feb;131(2):346-52.e1-3
pubmed: 23265859
Am J Respir Crit Care Med. 2019 May 1;199(9):1127-1138
pubmed: 30789747
JAMA. 2016 Feb 23;315(8):788-800
pubmed: 26903337
PLoS One. 2012;7(2):e32486
pubmed: 22389704
Infect Disord Drug Targets. 2011 Aug;11(4):413-23
pubmed: 21679139
J Oncol. 2017;2017:5035371
pubmed: 29075294
Am J Respir Crit Care Med. 2013 Nov 15;188(10):1193-201
pubmed: 24024497
MBio. 2015 Mar 03;6(2):e00037
pubmed: 25736890
Am J Reprod Immunol. 2019 Aug;82(2):e13147
pubmed: 31087436
Cell Host Microbe. 2015 May 13;17(5):704-15
pubmed: 25865368
Nat Microbiol. 2016 Apr 04;1:16031
pubmed: 27572644
Am J Respir Crit Care Med. 2018 Mar 1;197(5):621-631
pubmed: 29035085
Microbiome. 2016 Feb 11;4:7
pubmed: 26865050
Am J Respir Crit Care Med. 2016 Mar 1;193(5):504-15
pubmed: 26492486
Am J Respir Crit Care Med. 2014 Oct 15;190(8):906-13
pubmed: 25184687
PLoS One. 2016 Oct 5;11(10):e0163962
pubmed: 27706213
Am J Respir Crit Care Med. 2011 Oct 15;184(8):957-63
pubmed: 21680950
JAMA. 2012 Jun 20;307(23):2526-33
pubmed: 22797452
Mucosal Immunol. 2017 Mar;10(2):299-306
pubmed: 27966551
Am J Physiol Lung Cell Mol Physiol. 2015 Jul 1;309(1):L76-83
pubmed: 25957290
Microbiome. 2013 Jul 01;1(1):19
pubmed: 24450871
J Allergy Clin Immunol. 2018 Feb;141(2):718-729.e7
pubmed: 28729000
MBio. 2017 Feb 14;8(1):
pubmed: 28196961
Am J Respir Crit Care Med. 2019 May 15;199(10):1205-1213
pubmed: 30376356
Lancet Respir Med. 2014 Jul;2(7):548-56
pubmed: 24767767
Thorax. 2013 May;68(5):436-41
pubmed: 23321605
Thorax. 2015 Jul;70(7):636-46
pubmed: 25964315
Nat Methods. 2010 May;7(5):335-6
pubmed: 20383131
Sci Rep. 2018 Jan 12;8(1):568
pubmed: 29330443
J Immunol. 2016 Jun 15;196(12):4839-47
pubmed: 27260767