Tumor necrosis factor alpha increases intestinal permeability in mice with fulminant hepatic failure.

Aim: To determine the effect of tumor necrosis factor alpha (TNF-α) on intestinal permeability (IP) in mice with fulminant hepatic failure (FHF), and the expression of tight junction proteins.

Methods: We selected D-lactate as an index of IP, induced FHF using D-galactosamine/lipopolysaccharide and D-galactosamine/TNF-α, assessed the results using an enzymatic-spectrophotometric method, transmission electron microscopy, immunohistochemistry, Western blotting and real-time quantitative polymerase chain reaction. The effect of the administration of anti-TNF-α immunoglobulin G (IgG) antibody, before the administration of D-galactosamine/lipopolysaccharide, on TNF-α was also assessed.

Decreased IgA+ plasma cells and IgA expression in acute liver necrosis mice.

Aim: To investigate the number of intestinal immunoglobulin A (IgA+) plasma cells and expression of intestinal IgA in mice with acute liver necrosis.

Methods: A model of acute liver necrosis was established by intraperitoneal injection of galactosamine (GalN) and lipopolysaccharide (LPS). Sixty mice were randomly divided into one of 4 equal groups: normal control, acute liver necrosis, LPS, or GalN.

TNFα-induced IP3R1 expression through TNFR1/PC-PLC/PKCα and TNFR2 signalling pathways in human mesangial cell.

Background: Little information is available regarding the mechanisms involved in cytokine-induced type 1 inositol 1,4,5-trisphosphate receptor (IP(3)R1) expression in human mesangial cells (HMCs) in the occurrence of hepatorenal syndrome (HRS). Over-expression of IP(3)R1 would enhance both IP(3)-binding activity and sensitivity. We hypothesize that it is possible that increased IP(3)R1, induced by TNFα, would lead to increased IP(3) sensitivity in response to a variety of vasoconstrictors, and promote HMC contraction and thus lead to reduced GFP, promoting HRS occurrence and development.