Bacterial translocation occurs early in cirrhosis and triggers a selective inflammatory response

• DOI: 10.1007/s12072-023-10496-y
• Publication Date: 2023-03-07T13:03:36Z
• Authors: Benedikt Simbrunner; Esther Caparrós; Teresa Neuwirth; Philipp Schwabl; Philipp Königshofer; David Bauer; Rodrig Marculescu; Michael Trauner; Bernhard Scheiner; Georg Stary; Mattias Mandorfer; Thomas Reiberger; Rubén Francés
• Keywords: Decompensation

Experimental data suggest that bacterial translocation (BT) promotes systemic inflammation, portal hypertension, and circulatory dysfunction in advanced chronic liver disease (ACLD).Patients with ACLD undergoing hepatic venous pressure gradient (HVPG) measurement absence of acute decompensation or infections were included (n = 249). Serum biomarkers BT (lipopolysaccharide [LPS], lipoteichoic acid [LTA], DNA [bactDNA]), inflammation markers assessed. T-cell subsets intestinal biopsies 7 ACLD, n 4 controls) analyzed by flow cytometry.Patients had a median HVPG 18 (12-21) mmHg 56% decompensated ACLD. LPS (0.04 [0.02-0.06] vs. 0.64 [0.30-1.06] EU/mL), LTA (4.53 [3.58-5.97] 43.2 [23.2-109] pg/mL), detection bactDNA (≥ 5 pg/mL; 5% 41%) markedly higher patients than healthy controls 40; p < 0.001) but similar between different clinical stages compensated displayed no meaningful correlation hemodynamics. TNF-α IL-10 correlated (Spearman's rs 0.523, 0.001/rs 0.143, 0.024) not LTA. Presence was associated (0.54 [0.28-0.95] 0.88 [0.32-1.31] EU/mL, (15.3 [6.31-28.1] 20.9 [13.8-32.9] pg/mL). Patients exhibited decreased CD4:CD8-ratio increased TH1-cells the mucosa as compared to controls. During FU 14.7 (8.20-26.5) months, antigens did predict liver-related death (in contrast HVPG, IL-6, MAP) well at 24 months.BT occurs already early triggers inflammatory response via IL-10. Interestingly, showed clear hypertension stable ACLD.NCT03267615.