{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T03:02:42Z","timestamp":1791428562893,"version":"4.3.3"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2018,2,22]],"date-time":"2018-02-22T00:00:00Z","timestamp":1519257600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"},{"start":{"date-parts":[[2018,2,22]],"date-time":"2018-02-22T00:00:00Z","timestamp":1519257600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:p>\n                    Intestinal dysbiosis is implicated in alcoholic hepatitis (AH). However, changes in the circulating microbiome, its association with the presence and severity of AH, and its functional relevance in AH is unknown. Qualitative and quantitative assessment of changes in the circulating microbiome were performed by sequencing bacterial DNA in subjects with moderate AH (MAH) (n = 18) or severe AH (SAH) (n = 19). These data were compared with heavy drinking controls (HDCs) without obvious liver disease (n = 19) and non\u2013alcohol\u2010consuming controls (NACs, n = 20). The data were related to endotoxin levels and markers of monocyte activation. Linear discriminant analysis effect size (LEfSe) analysis, inferred metagenomics, and predictive functional analysis using PICRUSt were performed. There was a significant increase in 16S copies\/ng DNA both in MAH (\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    &lt; 0.01) and SAH (\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    &lt; 0.001) subjects. Compared with NACs, the relative abundance of phylum\n                    <jats:italic toggle=\"yes\">Bacteroidetes<\/jats:italic>\n                    was significantly decreased in HDCs, MAH, and SAH (\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    &lt; 0.001). In contrast, all alcohol\u2010consuming groups had enrichment with\n                    <jats:italic toggle=\"yes\">Fusobacteria<\/jats:italic>\n                    ; this was greatest for HDCs and decreased progressively in MAH and SAH. Subjects with SAH had significantly higher endotoxemia (\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    = 0.01). Compared with alcohol\u2010consuming groups, predictive functional metagenomics indicated an enrichment of bacteria with genes related to methanogenesis and denitrification. Furthermore, both HDCs and SAH showed activation of a type III secretion system that has been linked to gram\u2010negative bacterial virulence. Metagenomics in SAH versus NACs predicted increased isoprenoid synthesis via mevalonate and anthranilate degradation, known modulators of gram\u2010positive bacterial growth and biofilm production, respectively.\n                    <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic>\n                    Heavy alcohol consumption appears to be the primary driver of changes in the circulating microbiome associated with a shift in its inferred metabolic functions. (H\n                    <jats:sc>epatology<\/jats:sc>\n                    2018;67:1284\u20101302).\n                  <\/jats:p>","DOI":"10.1002\/hep.29623","type":"journal-article","created":{"date-parts":[[2017,10,30]],"date-time":"2017-10-30T11:38:47Z","timestamp":1509363527000},"page":"1284-1302","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":128,"title":["The circulating microbiome signature and inferred functional metagenomics in alcoholic hepatitis"],"prefix":"10.1097","volume":"67","author":[{"given":"Puneet","family":"Puri","sequence":"first","affiliation":[{"name":"Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine,Virginia Commonwealth University,Richmond,VA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suthat","family":"Liangpunsakul","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana 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Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Borst","sequence":"additional","affiliation":[{"name":"Department of Biostatistics,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qigui","family":"Yu","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Divya P.","family":"Kumar","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine,Virginia Commonwealth University,Richmond,VA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faridoddin","family":"Mirshahi","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine,Virginia 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