title: Survival and cellular immune functions in septic mice treated with growth hormone (GH) and insulin-like growth factor-I (IGF-I).
abstract: OBJECTIVE
  GH was used to counteract the catabolic metabolism in critically ill patients until it was demonstrated that administration of GH was associated with an increased morbidity due to uncontrolled infections and sepsis. The immunomodulatory effect of GH and its main mediator IGF-I during systemic inflammation remain to be established. We therefore investigated the effect of GH and IGF-I on cellular immune functions in a murine model of sepsis.
  
  
  METHODS
  Randomized animal study. Septic mice were treated with either saline, GH (1mg/kg/24h s.c.), IGF-I (4mg/kg/24h), or GH in combination with IGF-I over a 48h period.
  
  
  METHODS
  Level 1 trauma center, university research laboratory.
  
  
  OBJECTIVE
  Male NMRI mice.
  
  
  METHODS
  clinical parameters (survival rate, body weight, body temperature, fluid intake, food intake, blood glucose levels) and cellular immune functions (splenocyte proliferation by using a (3)H-thymidine incorporation assay, splenocyte apoptosis by determination of Annexin V binding capacity, splenocyte IL-2, IL-6, and TNF-alpha release by using ELISA, and distribution of circulating immune cell subsets by FACScan).
  
  
  RESULTS
  Administration of GH did not affect clinical parameters or cellular immune functions in septic mice. In contrast, treatment with IGF-I alone or in combination with GH improved splenocyte proliferation and increased the ability of splenocytes to release IL-2 and IL-6 without affecting the survival rate or any other clinical parameter determined.
  
  
  CONCLUSIONS
  GH did not affect cellular immune functions or the survival rate in our murine sepsis model. In contrast, IGF-I improved splenocyte proliferation and cytokine release independently of GH but did not affect the determined clinical parameters of septic mice.
authors.affiliation: Department of Trauma Surgery, University Hospital of Essen, Hufelandstrasse 55, 45147 Essen, Germany.
authors.forename: Daniel
authors.initials: D
authors.lastname: Schmitz
authors.forename: Phillip
authors.initials: P
authors.lastname: Kobbe
authors.forename: Sven
authors.initials: S
authors.lastname: Lendemanns
authors.forename: Klaus
authors.initials: K
authors.lastname: Wilsenack
authors.forename: Michael
authors.initials: M
authors.lastname: Exton
authors.forename: Manfred
authors.initials: M
authors.lastname: Schedlowski
authors.forename: Reiner
authors.initials: R
authors.lastname: Oberbeck
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D016207:Cytokines / Q000276:immunology; D013006:Growth Hormone / Q000494:pharmacology*; D007111:Immunity, Cellular / Q000187:drug effects*; D007958:Leukocyte Count; D008297:Male; D051379:Mice; D011897:Random Allocation; D018805:Sepsis / Q000276:immunology*; D013002:Somatomedins / Q000494:pharmacology*; D013154:Spleen / Q000166:cytology / Q000187:drug effects; D016019:Survival Analysis
chemical_list: D016207:Cytokines; D013002:Somatomedins; D013006:Growth Hormone