Fig. 5.

Monocyte dysfunction in decompensated cirrhosis.

Geometric MFI of HLA-DR cell surface expression on (A) all monocytic cells, (B) classical, and (C) intermediate monocytes in n = 11, 10, and 24 for HVs, OPDs, and AD/ACLF, respectively. (D) Monocyte HLA-DR expression by flow cytometry following incubation of HV whole blood ±1 ng/ml of PGE₂ for 72 h (n = 3). TNFα (E) and IL6 (F) expression in HV monocytes following LPS stimulation. (G) TNFα and (H) IL6 at 4 h in n = 21, 11, and 28 for HVs, OPDs, and AD/ACLF, respectively, with the log [TNFα/IL6 normalised to monocyte number] displayed. Correlation between baseline MFI HLA-DR expression on CM cell population with subsequent whole blood (I) TNFα and (J) IL6 production following LPS stimulation (n = 9, 11, and 28 for HVs, OPDs, and AD/ACLF, respectively). (K) Correlation between LPS-stimulated monocyte TNFα production and serum albumin in decompensated cirrhosis. (L) MFI of CD64 cell surface expression on all monocytic cells in n = 11, 10, and 24 for HVs, OPDs, and AD/ACLF, respectively. Individual data points or mean ± SEM shown with 1-way ANOVA with Tukey multiple comparisons test (all groups compared) or unpaired t-test when 2 groups. ∗p <0.05, ∗∗p <0.01, ∗∗∗p <0.001, ∗∗∗∗p <0.0001. ACLF, acute-on-chronic liver failure; AD, acute decompensation; CM, classical monocytes; HLA-DR, human leukocyte antigen – DR isotype; HVs, healthy volunteers; LPS, lipopolysaccharide; MFI, mean fluorescence intensity; PGE₂, prostaglandin E₂; OPD, patients with refractory ascites attending hospital outpatient department for day-case paracentesis; TNFα, tumour necrosis factor alpha.