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Hepatic encephalopathy (HE) is the neuropsychiatric complication of liver cirrhosis (LC). The influence of gut microbiota on HE pathogenesis has been suggested but not precisely elucidated. Here, we investigate how the gut microbial profile changed in patients with HE to clarify the functional gut microbial species associated with HE. We focused on their responses to rifaximin (RFX), a nonabsorbable antibiotic used in HE therapy. Feces samples were collected from patients with decompensated LC (all HE), patients with compensated LC, and healthy controls, and fecal gut microbial profiles were compared using 16S ribosomal RNA gene amplicon and metagenomic sequencing. The linear discriminant analysis effect size was used to identify specific species.  Urease ‐positive  Streptococcus salivarius , which can produce ammonia, was identified as the most significantly abundant gut microbiota in the HE group, and its ability to elevate the levels of blood ammonia as well as brain glutamine was experimentally verified in mice.  Urease ‐negative  Ruminococcus gnavus  was also identified as a significantly abundant species in patients with RFX‐nonresponsive HE after RFX administration. Interestingly,  R .  gnavus  enhanced urease activity of recombinant urease itself, implying that  R .  gnavus  could amplify ammonia production of surrounding  urease ‐positive microbiota. Furthermore, the sensitivity of  S. salivarius  and  R .  gnavus  to RFX depended on conjugated secondary bile acid levels, suggesting a therapeutic potential of the combined use of secondary bile acid levels with RFX for enhancing the efficacy of RFX. This study identified specific gut bacterial species abundant in patients with HE and verified their functions linked to HE pathophysiology. Targeting these bacteria could be a potentially effective strategy to treat HE.

Distinct responsiveness to rifaximin in patients with hepatic encephalopathy depends on functional gut microbial species