title: Soluble ST2 protein in cardiac surgery: a possible negative feedback loop to prevent uncontrolled inflammatory reactions.
abstract: BACKGROUND
  Recent reports have demonstrated that cardiopulmonary bypass (CBP) utilization leads to a TH2 cytokine bias in patients undergoing coronary artery bypass grafting (CABG) operation. The relation of soluble ST2 and secretion of IL-10, markers of TH2 T-cell activation, and IL-13 in relation to immunoglobulin isotope production is not known in patients undergoing On- versus Off-pump (CABG) procedure.
  
  
  METHODS
  30 patients were prospectively included in the study (On- vs Off-pump CABG, each n = 15). Serum samples were obtained prior to, and 30 min, 60 min and 24hrs after operation. ELISA was utilized to detect sST2 and IL-10, IL-13 and immunoglobulin isotype production.
  
  
  RESULTS
  In both cohorts we could demonstrate a significant rise of ST2 24 hours after the CABG procedure. In the On-pump group ST2 levels (pg/ml) before the operation, at 30 and 60 minutes and after 24 hours were 115.3 +/- 25, 71.2 +/- 15, 114.1 +/- 26 and 4231.9 +/- 520, respectively. In the Off-pump group they were 200.3 +/- 109, 91.2 +/- 20, 137 +/- 29 and 4144.9 +/- 488 (both, p < 0.0001, p < 0.0001, respectively). IL-10 (pg/ml) levels rose from preoperative values of 6.2 +/- 1.6 in the On-pump group and 7.91 +/- 1.8 in the Off-pump group to 33.14 +/- 8.7 and 13.72 +/- 3 after 60 minutes (p 0.0189, p 0.0397, respectively). IL-13 levels and immunoglobulin production did not change significantly within the study period irrespective of the operation procedure used.
  
  
  CONCLUSIONS
  In conclusion, our results demonstrate that sST2 and IL-10, markers of TH2 cytokine producing cells, are increased in CABG operation, irrespective of the procedure selected, and settles a longstanding controversy concerning the shift from Th1 to Th2 cells.
authors.affiliation: Department of Cardiac Surgery, University of Debrecen, Debrecen, Hungary.
authors.forename: Tamás
authors.initials: T
authors.lastname: Szerafin
authors.forename: Markus
authors.initials: M
authors.lastname: Brunner
authors.forename: Ambrus
authors.initials: A
authors.lastname: Horváth
authors.forename: Lajos
authors.initials: L
authors.lastname: Szentgyörgyi
authors.forename: Bernhard
authors.initials: B
authors.lastname: Moser
authors.forename: George
authors.initials: G
authors.lastname: Boltz-Nitulescu
authors.forename: Arpád
authors.initials: A
authors.lastname: Péterffy
authors.forename: Konrad
authors.initials: K
authors.lastname: Hoetzenecker
authors.forename: Barbara
authors.initials: B
authors.lastname: Steinlechner
authors.forename: Ernst
authors.initials: E
authors.lastname: Wolner
authors.forename: Hendrik Jan
authors.initials: HJ
authors.lastname: Ankersmit
mesh_terms: D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D003327:Coronary Disease / Q000601:surgery*; D004797:Enzyme-Linked Immunosorbent Assay; D025461:Feedback, Physiological / Q000502:physiology*; D005260:Female; D006801:Humans; D007132:Immunoglobulin Isotypes / Q000097:blood; D000072179:Interleukin-1 Receptor-Like 1 Protein; D016753:Interleukin-10 / Q000097:blood; D018793:Interleukin-13 / Q000097:blood; D008213:Lymphocyte Activation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000097:blood* / Q000276:immunology; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism; D013997:Time Factors
chemical_list: C079241:IL1RL1 protein, human; D007132:Immunoglobulin Isotypes; D000072179:Interleukin-1 Receptor-Like 1 Protein; D018793:Interleukin-13; D011956:Receptors, Cell Surface; D016753:Interleukin-10