: Metabolic dysfunction-associated steatotic liver disease (MASLD), driven by obesity and metabolic syndrome, is increasingly prevalent and a significant contributor to liver fibrosis, cirrhosis, and liver-related mortality. Emerging research implicates the gut microbiome as a critical player in MASLD progression, yet specific microbial drivers remain poorly understood. Here, we explore the role of () in MASLD progression through both human patient cohorts and a mouse model of diet-induced obesity. : Using 16S rRNA sequencing, we identified elevated abundance in MASLD patients with advanced fibrosis, linked with significant shifts in microbial diversity and bacterial network connectivity. To investigate causality, experimental colonization of in mice on a high-fat diet worsened MASLD progression, with -colonized mice showing significant increases in hepatic steatosis, liver triglyceride accumulation, and body weight, independent of caloric intake. At the molecular level, colonization downregulated key lipid metabolism genes, such as carnitine palmitoyltransferase 1 and adipose triglyceride lipase, and impaired tight intestinal junction integrity through the downregulation of occludin. Collectively, our findings position as a possible driver of MASLD progression by promoting hepatic steatosis through lipid and triglyceride accumulation and fibrosis through decreased tight junction integrity. These insights suggest a promising therapeutic avenue to target specific microbial signatures like to curb MASLD progression and mitigate the associated risk of advanced fibrosis.