Schmidt AI, Kühlbrey C, Lauch R et al.
Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
Pancreatology : official journal of the International Association of Pancreatology (IAP) … [et al.]. Feb 2017.
In necrotizing acute pancreatitis (NAP), systemic inflammatory response syndrome (SIRS) and the compensatory anti-inflammatory response syndrome (CARS) decide overall outcome and mortality. In patients, low lymphocyte counts were found, but T-helper cells seemed to conversely increase. Our aim was to further categorize T-helper cells within the context of NAP induced SIRS and CARS.NAP was induced by injection of sodium-taurocholate into the common bile duct of male BALB/c mice; sham treated animals received saline infusion. The animals were sacrificed at 6, 12, 24 and 48 h later. Lymphocytes from blood, liver and spleen were isolated and examined by flow cytometry. Staining was performed for CD4, CD8, CD19, CD45RB, CD25, CD69, and CD152. CD4(+) cells were sorted for their CD45RB expression and sought for gene regulation associated to TH1/TH2 cells by quantitative RT-PCR.In NAP, CD4(+) was solely increased in all compartments. CD8(+) remained without substantial alterations. CD45RB showed significant expression in RB(high) in T-helper cells, confirmed by the CD45RB(high/low) ratio (Liver, 24 h: NAP 2.2, SHAM 0.6; p < 0.001). CD45RB(high) and (-low) cells were not associated to patterns of TH1/TH2 expression. In NAP, CCR4 expression was significantly decreased within RB(high) cells (fold change: 0.04, p < 0.05), while TLR6 showed significant overexpression (fold change: 2.36, p < 0.05).T-helper cells increase in NAP, leaning towards CD45RB(high) expression. They resemble naive T-cells, in which NAP leads to expression profiles associated with an innate immune response. This suggests new findings in immunological pathomechanisms of NAP. Pubmed