Gut microbiota analysis and its significance in vasovagal syncope in children.
Journal
Chinese medical journal
ISSN: 2542-5641
Titre abrégé: Chin Med J (Engl)
Pays: China
ID NLM: 7513795
Informations de publication
Date de publication:
Feb 2019
Feb 2019
Historique:
pubmed:
2
2
2019
medline:
1
6
2019
entrez:
2
2
2019
Statut:
ppublish
Résumé
Vasovagal syncope (VVS) is common in children and greatly affect both physical and mental health. But the mechanisms have not been completely explained. This study was designed to analyze the gut microbiota in children with VVS and explore its clinical significance. Fecal samples from 20 VVS children and 20 matched controls were collected, and the microbiota were analyzed by 16S rRNA gene sequencing. The diversity and microbiota compositions of the VVS cases and controls were compared with the independent sample t test or Mann-Whitney U test. The correlation between the predominant bacteria and clinical symptoms was analyzed using Pearson or Spearman correlation test. No significant differences in diversity were evident between VVS and controls (P > 0.05). At the family level, the relative abundance of Ruminococcaceae was significantly higher in VVS children than in controls (median [Q1, Q3]: 22.10% [16.89%, 27.36%] vs. 13.92% [10.31%, 20.18%], Z = -2.40, P < 0.05), and LEfSe analysis revealed Ruminococcaceae as a discriminative feature (linear discriminant analysis [LDA] score > 4, P < 0.05). The relative abundance of Ruminococcaceae in VVS patients was positively correlated with the frequency of syncope (r = 0.616, P < 0.01). In terms of its correlation with hemodynamics, we showed that relative abundance of Ruminococcaceae was negatively correlated with the systolic and diastolic pressure reduction at the positive response in head-up tilt test (HUTT; r = -0.489 and -0.448, all P < 0.05), but was positively correlated with the mean pressure drop and decline rate (r = 0.489 and 0.467, all P < 0.05) as well as diastolic pressure drop and decline rate at the HUTT positive response (r = 0.579 and 0.589, all P < 0.01) in VVS patients. Ruminococcaceae was the predominant gut bacteria and was associated with the clinical symptoms and hemodynamics of VVS, suggesting that gut microbiota might be involved in the development of VVS.
Sections du résumé
BACKGROUND
BACKGROUND
Vasovagal syncope (VVS) is common in children and greatly affect both physical and mental health. But the mechanisms have not been completely explained. This study was designed to analyze the gut microbiota in children with VVS and explore its clinical significance.
METHODS
METHODS
Fecal samples from 20 VVS children and 20 matched controls were collected, and the microbiota were analyzed by 16S rRNA gene sequencing. The diversity and microbiota compositions of the VVS cases and controls were compared with the independent sample t test or Mann-Whitney U test. The correlation between the predominant bacteria and clinical symptoms was analyzed using Pearson or Spearman correlation test.
RESULTS
RESULTS
No significant differences in diversity were evident between VVS and controls (P > 0.05). At the family level, the relative abundance of Ruminococcaceae was significantly higher in VVS children than in controls (median [Q1, Q3]: 22.10% [16.89%, 27.36%] vs. 13.92% [10.31%, 20.18%], Z = -2.40, P < 0.05), and LEfSe analysis revealed Ruminococcaceae as a discriminative feature (linear discriminant analysis [LDA] score > 4, P < 0.05). The relative abundance of Ruminococcaceae in VVS patients was positively correlated with the frequency of syncope (r = 0.616, P < 0.01). In terms of its correlation with hemodynamics, we showed that relative abundance of Ruminococcaceae was negatively correlated with the systolic and diastolic pressure reduction at the positive response in head-up tilt test (HUTT; r = -0.489 and -0.448, all P < 0.05), but was positively correlated with the mean pressure drop and decline rate (r = 0.489 and 0.467, all P < 0.05) as well as diastolic pressure drop and decline rate at the HUTT positive response (r = 0.579 and 0.589, all P < 0.01) in VVS patients.
CONCLUSION
CONCLUSIONS
Ruminococcaceae was the predominant gut bacteria and was associated with the clinical symptoms and hemodynamics of VVS, suggesting that gut microbiota might be involved in the development of VVS.
Identifiants
pubmed: 30707176
doi: 10.1097/CM9.0000000000000086
pmc: PMC6595724
doi:
Substances chimiques
Fatty Acids, Volatile
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
411-419Références
World J Gastroenterol. 2002 Jun;8(3):540-5
pubmed: 12046088
Circulation. 2002 Jul 30;106(5):569-74
pubmed: 12147538
Neuroscience. 2003;119(1):215-21
pubmed: 12763082
J Pediatr. 2004 Aug;145(2):223-8
pubmed: 15289772
J Cardiovasc Electrophysiol. 2006 Jan;17(1):49-54
pubmed: 16426400
J Clin Gastroenterol. 2006 Mar;40(3):235-43
pubmed: 16633129
Nature. 2008 Oct 23;455(7216):1109-13
pubmed: 18806780
Nat Rev Gastroenterol Hepatol. 2009 May;6(5):306-14
pubmed: 19404271
Auton Neurosci. 2010 Feb 16;153(1-2):41-6
pubmed: 19674941
J Appl Physiol (1985). 2010 Mar;108(3):523-32
pubmed: 20056846
ISME J. 2011 Feb;5(2):169-72
pubmed: 20827291
Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):18933-8
pubmed: 20937875
Nature. 2011 Apr 7;472(7341):57-63
pubmed: 21475195
Genome Biol. 2011 Jun 24;12(6):R60
pubmed: 21702898
J Nutr. 2012 Jul;142(7):1259-65
pubmed: 22649263
Nat Rev Microbiol. 2012 Nov;10(11):735-42
pubmed: 23000955
PLoS One. 2012;7(10):e46231
pubmed: 23056268
Water Res. 2013 Sep 1;47(13):4207-16
pubmed: 23764571
Gut. 2014 Dec;63(12):1913-20
pubmed: 25021423
Pacing Clin Electrophysiol. 2014 Dec;37(12):1694-701
pubmed: 25139789
Hypertension. 2015 Jun;65(6):1331-40
pubmed: 25870193
Redox Biol. 2015 Aug;5:398-408
pubmed: 26163808
Sci Rep. 2015 Aug 03;5:12676
pubmed: 26234821
Nat Rev Microbiol. 2016 Jan;14(1):20-32
pubmed: 26499895
Zhonghua Er Ke Za Zhi. 2016 Apr;54(4):246-50
pubmed: 27055420
Europace. 2017 Jan;19(1):127-131
pubmed: 27702846
Heart. 2017 Nov;103(21):1711-1718
pubmed: 28501796
J Hypertens. 2017 Sep;35(9):1899-1908
pubmed: 28509726
Neuroepidemiology. 2017;49(1-2):31-33
pubmed: 28810256