The gut microbiome distinguishes mortality in trauma patients upon admission to the emergency department.
Adult
Aged
Emergency Service, Hospital
/ statistics & numerical data
Feces
/ microbiology
Female
Follow-Up Studies
Gastrointestinal Microbiome
/ physiology
Hospital Mortality
Humans
Injury Severity Score
Length of Stay
/ statistics & numerical data
Male
Middle Aged
Prognosis
Prospective Studies
Trauma Centers
/ statistics & numerical data
Wounds, Nonpenetrating
/ diagnosis
Wounds, Penetrating
/ diagnosis
Journal
The journal of trauma and acute care surgery
ISSN: 2163-0763
Titre abrégé: J Trauma Acute Care Surg
Pays: United States
ID NLM: 101570622
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
pubmed:
11
2
2020
medline:
28
8
2020
entrez:
11
2
2020
Statut:
ppublish
Résumé
Traumatic injury can lead to a compromised intestinal epithelial barrier, decreased gut perfusion, and inflammation. While recent studies indicate that the gut microbiome (GM) is altered early following traumatic injury, the impact of GM changes on clinical outcomes remains unknown. Our objective of this follow-up study was to determine if the GM is associated with clinical outcomes in critically injured patients. We conducted a prospective, observational study in adult patients (N = 67) sustaining severe injury admitted to a level I trauma center. Fecal specimens were collected on admission to the emergency department, and microbial DNA from all samples was analyzed using the Quantitative Insights Into Microbial Ecology pipeline and compared against the Greengenes database. α-Diversity and β-diversity were estimated using the observed species metrics and analyzed with t tests and permutational analysis of variance for overall significance, with post hoc pairwise analyses. Our patient population consisted of 63% males with a mean age of 44 years. Seventy-eight percent of the patients suffered blunt trauma with 22% undergoing penetrating injuries. The mean body mass index was 26.9 kg/m. Significant differences in admission β-diversity were noted by hospital length of stay, intensive care unit hospital length of stay, number of days on the ventilator, infections, and acute respiratory distress syndrome (p < 0.05). β-Diversity on admission differed in patients who died compared with patients who lived (mean time to death, 8 days). There were also significantly less operational taxonomic units in samples from patients who died versus those who survived. A number of species were enriched in the GM of injured patients who died, which included some traditionally probiotic species such as Akkermansia muciniphilia, Oxalobacter formigenes, and Eubacterium biforme (p < 0.05). Gut microbiome diversity on admission in severely injured patients is predictive of a variety of clinically important outcomes. While our study does not address causality, the GM of trauma patients may provide valuable diagnostic and therapeutic targets for the care of injured patients. Prognostic and epidemiological, level III.
Sections du résumé
BACKGROUND
Traumatic injury can lead to a compromised intestinal epithelial barrier, decreased gut perfusion, and inflammation. While recent studies indicate that the gut microbiome (GM) is altered early following traumatic injury, the impact of GM changes on clinical outcomes remains unknown. Our objective of this follow-up study was to determine if the GM is associated with clinical outcomes in critically injured patients.
METHODS
We conducted a prospective, observational study in adult patients (N = 67) sustaining severe injury admitted to a level I trauma center. Fecal specimens were collected on admission to the emergency department, and microbial DNA from all samples was analyzed using the Quantitative Insights Into Microbial Ecology pipeline and compared against the Greengenes database. α-Diversity and β-diversity were estimated using the observed species metrics and analyzed with t tests and permutational analysis of variance for overall significance, with post hoc pairwise analyses.
RESULTS
Our patient population consisted of 63% males with a mean age of 44 years. Seventy-eight percent of the patients suffered blunt trauma with 22% undergoing penetrating injuries. The mean body mass index was 26.9 kg/m. Significant differences in admission β-diversity were noted by hospital length of stay, intensive care unit hospital length of stay, number of days on the ventilator, infections, and acute respiratory distress syndrome (p < 0.05). β-Diversity on admission differed in patients who died compared with patients who lived (mean time to death, 8 days). There were also significantly less operational taxonomic units in samples from patients who died versus those who survived. A number of species were enriched in the GM of injured patients who died, which included some traditionally probiotic species such as Akkermansia muciniphilia, Oxalobacter formigenes, and Eubacterium biforme (p < 0.05).
CONCLUSION
Gut microbiome diversity on admission in severely injured patients is predictive of a variety of clinically important outcomes. While our study does not address causality, the GM of trauma patients may provide valuable diagnostic and therapeutic targets for the care of injured patients.
LEVEL OF EVIDENCE
Prognostic and epidemiological, level III.
Identifiants
pubmed: 32039976
doi: 10.1097/TA.0000000000002612
pii: 01586154-202005000-00001
pmc: PMC7905995
mid: NIHMS1554022
doi:
Types de publication
Journal Article
Observational Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
579-587Subventions
Organisme : NCATS NIH HHS
ID : KL2 TR002646
Pays : United States
Références
Nature. 2012 Nov 1;491(7422):119-24
pubmed: 23128233
J Trauma Acute Care Surg. 2019 Apr;86(4):573-582
pubmed: 30633104
Curr Opin Microbiol. 2014 Feb;17:67-74
pubmed: 24581695
Front Microbiol. 2017 Jul 06;8:1237
pubmed: 28729860
Dig Dis Sci. 2011 Apr;56(4):1171-7
pubmed: 20931284
mSystems. 2019 May 14;4(4):
pubmed: 31098397
Trauma Surg Acute Care Open. 2017 Oct 23;2(1):e000108
pubmed: 29766103
Burns. 2015 May;41(3):e28-33
pubmed: 25465986
J Trauma. 1996 Apr;40(4):501-10; discussion 510-2
pubmed: 8614027
ISME J. 2011 Feb;5(2):169-72
pubmed: 20827291
J Trauma. 1999 Nov;47(5):923-7
pubmed: 10568723
Dig Dis Sci. 2011 Aug;56(8):2361-5
pubmed: 21384123
Nutrition. 2018 Jan;45:104-107
pubmed: 29129229
Nat Rev Gastroenterol Hepatol. 2011 Aug 16;8(9):523-31
pubmed: 21844910
PLoS One. 2017 Feb 9;12(2):e0171579
pubmed: 28182644
J Am Coll Surg. 2018 May;226(5):719-729
pubmed: 29505823
Shock. 2019 Aug;52(2):240-248
pubmed: 29953417
Nat Rev Genet. 2012 Mar 13;13(4):260-70
pubmed: 22411464
Methods Mol Biol. 2018;1856:141-156
pubmed: 30178250
J Exp Med. 2016 Nov 14;213(12):2603-2620
pubmed: 27810921
Arch Med Res. 2017 Nov;48(8):727-734
pubmed: 29221800
Cell Host Microbe. 2012 Oct 18;12(4):496-508
pubmed: 23084918
Science. 2012 Jun 8;336(6086):1268-73
pubmed: 22674334
Cell. 2004 Jul 23;118(2):229-41
pubmed: 15260992
Am J Surg. 2018 Oct;216(4):699-705
pubmed: 30100050
Nature. 2013 Jul 4;499(7456):97-101
pubmed: 23803760
PLoS One. 2015 Jul 08;10(7):e0129996
pubmed: 26154283
Nat Rev Immunol. 2009 May;9(5):313-23
pubmed: 19343057
Brain Behav Immun. 2016 Oct;57:10-20
pubmed: 27060191