title: The predominance of a naive T helper cell subset in the immune response of experimental acute pancreatitis.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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/TH2cells by quantitative RT-PCR.
  
  
  RESULTS
  In NAP, CD4+was solely increased in all compartments. CD8+remained without substantial alterations. CD45RB showed significant expression in RBhighin T-helper cells, confirmed by the CD45RBhigh/lowratio (Liver, 24 h: NAP 2.2, SHAM 0.6; p < 0.001). CD45RBhighand-lowcells were not associated to patterns of TH1/TH2expression. In NAP, CCR4 expression was significantly decreased within RBhighcells (fold change: 0.04, p < 0.05), while TLR6 showed significant overexpression (fold change: 2.36, p < 0.05).
  
  
  CONCLUSIONS
  T-helper cells increase in NAP, leaning towards CD45RBhighexpression. 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.
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
authors.forename: Andrea I
authors.initials: AI
authors.lastname: Schmidt
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Kühlbrey
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
authors.forename: Robert
authors.initials: R
authors.lastname: Lauch
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
authors.forename: Guido
authors.initials: G
authors.lastname: Wolff-Vorbeck
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
authors.forename: Sophia
authors.initials: S
authors.lastname: Chikhladze
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany.
authors.forename: Ulrich T
authors.initials: UT
authors.lastname: Hopt
authors.affiliation: Department of General and Visceral Surgery, Universitätsklinik Freiburg, Freiburg, Germany. Electronic address: uwe.wittel@uniklinik-freiburg.de.
authors.forename: Uwe A
authors.initials: UA
authors.lastname: Wittel
mesh_terms: D000818:Animals; D015415:Biomarkers; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010195:Pancreatitis / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000145:classification / Q000502:physiology*
chemical_list: D015415:Biomarkers
keywords: CARS; CD45RB(high); Innate immunity; Lymphocyte suppression; Sepsis