Microbial signature of plaque and gut in acute coronary syndrome

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作者
Eugenia Pisano
Francesca Bugli
Anna Severino
Daniela Pedicino
Francesco Paroni Sterbini
Cecilia Martini
Flavio De Maio
Ramona Vinci
Andrea Sacconi
Francesco Canonico
Alessia D’Aiello
Alice Bonanni
Luca Proto
Pellegrino Ciampi
Myriana Ponzo
Maria Chiara Grimaldi
Andrea Urbani
Aniello Primiano
Jacopo Gervasoni
Rocco Montone
Filippo Crea
Maurizio Sanguinetti
Giovanna Liuzzo
机构
[1] Fondazione Policlinico Universitario A. Gemelli IRCCS,Department of Cardiovascular Sciences
[2] Catholic University of the Sacred Heart,Department of Cardiovascular and Pulmonary Sciences
[3] Fondazione Policlinico Universitario A. Gemelli IRCCS,Department of Laboratory and Infectious Sciences
[4] Catholic University of the Sacred Heart,Department of Basic Biotechnological Sciences, Intensivological and Perioperative Clinics
[5] Regina Elena National Cancer Institute- IRCCS,UOSD Clinical Trial Center, Biostatistics and Bioinformatics
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摘要
Gut microbiota is an emerging editable cardiovascular risk factor. We aim to investigate gut and coronary plaque microbiota, using fecal samples and angioplasty balloons from patients with acute coronary syndrome (ACS), chronic coronary syndrome (CCS) and control subjects. We examined bacterial communities in gut and coronary plaques by 16S rRNA sequencing and we performed droplet digital PCR analysis to investigate the gut relative abundance of the bacterial genes CutC/CntA involved in trimethylamine N-oxide synthesis. Linear discriminant analysis effect size (LEfSe) at the genus and species levels displayed gut enrichment in Streptococcus, Granulicatella and P. distasonis in ACS compared with CCS and controls; Roseburia, C. aerofaciens and F. prausnitzii were more abundant in controls than in patients. Principal component analysis (PCA) of 41 differentially abundant gut taxa showed a clustering of the three groups. In coronary plaque, LEfSe at the genus level revealed an enrichment of Staphylococcus and Streptococcus in ACS, and Paracoccus in CCS, whereas PCA of 15 differentially abundant plaque taxa exhibited clustering of ACS and CCS patients. CutC and CntA genes were more abundant in ACS and CCS than in controls while no significant difference emerged between ACS and CCS. Our results indicate that ACS and CCS exhibit a different gut and plaque microbial signature, suggesting a possible role of these microbiotas in coronary plaque instability.
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