Gut microbiota and innate immune barrier dysfunction in hepatic portal venous gas: a hypothesis-generating review.

Hepatic portal venous gas (HPVG) is an uncommon radiographic sign whose prognosis is driven by bowel necrosis and shock rather than by intraportal gas. Immunological events along the gut-liver axis have not been synthesized for adult HPVG, and dedicated microbiome, metabolomic, gut-vascular barrier (GVB), and immune-profiling data are lacking. This hypothesis-generating review proposes gut dysbiosis as a putative contributor to mucosal and hepatic innate immune failure, inferred from cirrhosis, porto-sinusoidal vascular disease (PSVD), and intestinal ischemia/reperfusion. In those proxy states, loss of acetyl-CoA butyrate-production capacity, context-dependent bile-acid shifts, lipopolysaccharide-Toll-like receptor 4 priming, facultative-anaerobe expansion, and fermentative H2/CO2 pathways documented in cultured HPVG isolates-Clostridium perfringens (pyruvate-ferredoxin oxidoreductase-hydrogenase) and Escherichia coli (pyruvate-formate lyase-formate hydrogen lyase)-compromise epithelial and GVB integrity. These links are not assembled as a demonstrated sequence in adult HPVG. We propose a physical-core model in which a route of entry and a local driving pressure gradient are necessary, whereas pathway-defined fermentative isolates, dysbiosis, mucosal inflammation, ischemia, and impaired portal clearance are optional amplifiers. Iatrogenic or purely pressure-related HPVG can occur without dysbiosis or a substantial pathogen-associated molecular pattern load; in necrosis-driven HPVG, dysbiosis is proposed only as a concurrent immune amplifier; when HPVG occurs in cirrhosis or PSVD, portal hypertension is treated as a host modifier of barrier geometry and washout, not as an independent generator of intraportal gas. Portal vein thrombosis, portal hypertension, pneumatosis intestinalis, pyogenic liver abscess, and HPVG may share the portal vein as a conduit but are not interchangeable. No microbiota-directed intervention has been tested against an HPVG endpoint and none should delay source control; probiotics, rifaximin, fecal microbiota transplantation, diet, and phage remain research questions.