Lower gut microbiome diversity and higher abundance of proinflammatory genus <i>Collinsella</i> are associated with biopsy-proven nonalcoholic steatohepatitisOriginal paper
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreWhat was studied?
This study examined whether gut microbiome composition differs in people with biopsy-proven nonalcoholic steatohepatitis (NASH), the more severe, inflammatory form of nonalcoholic fatty liver disease (NAFLD) that can progress to cirrhosis. Researchers characterized microbial diversity and specific genus-level abundances in NASH patients, both with and without cirrhosis, and compared these to healthy controls. They also tested whether the most NASH-associated genus correlated with blood lipid markers such as triglycerides and cholesterol.
Who was studied?
The study included UK patients with biopsy-confirmed NASH, split into those without cirrhosis (n = 40) and those with cirrhosis (n = 25), for a combined NASH group of 65 patients. These were compared against 76 healthy controls. All participants had their gut microbiome composition assessed, alongside fasting lipid measurements in at least some individuals.
What were the most important findings?
NASH patients without cirrhosis showed a 7% lower Shannon alpha diversity than controls, and this dropped further to 14% lower in NASH patients with cirrhosis, indicating progressively reduced microbial diversity with disease severity. Beta diversity (unweighted UniFrac distance) was also significantly reduced in both NASH groups compared to controls. The genus Collinsella was most strongly associated with NASH, rising from 0.29% abundance in controls to 3.45% in NASH without cirrhosis and 4.38% in NASH with cirrhosis. Collinsella abundance was also positively correlated with fasting triglycerides and total cholesterol, and negatively correlated with high-density lipoprotein cholesterol.
What are the greatest implications of this study?
These findings strengthen the case that reduced gut microbial diversity and enrichment of specific proinflammatory taxa, particularly Collinsella, are linked to NASH severity and associated lipid abnormalities. Because Collinsella has previously been tied to obesity and atherosclerosis, its elevation in NASH suggests a potentially shared microbial pathway across these metabolic conditions. This supports gut microbiome composition, and Collinsella abundance specifically, as a candidate biomarker or contributor to NASH pathogenesis worth further mechanistic investigation.