title: Influence of selective decontamination of the digestive tract on cell-mediated immune function and bacteria/endotoxin translocation in thermally injured rats.
abstract: OBJECTIVE
  To determine the influence of pretreatment with selective decontamination of the digestive tract (SDD) on systemic immunosuppression, and the relationship between bacteria/endotoxin translocation and abnormalities of immune function in thermally injured rats.
  
  
  METHODS
  Animals were subjected to a 40% full-thickness scald injury, and divided into SDD-treated and control groups. The treatment group received SDD (polymyxin E, tobramycin, and 5-flucytosine) by gavage twice daily for 3 days before the experiment and continued for 5 days after thermal injury. The control group was given the same amount of water. The parameters reflecting cell-mediated immunity, including splenocyte proliferation in response to mitogens, interleukin 2 (IL-2) production, and lymphocyte subpopulation, were measured before injury and 1 and 5 days after burn, respectively.
  
  
  RESULTS
  Thermal injury resulted in marked reduction in splenocyte proliferative response to T-cell mitogens, IL-2 production, and T-helper/suppressor cells (CD4/CD8) ratio. Prophylactic treatment with SDD significantly decreased the incidences of bacterial translocation and endotoxemia, prevented suppressive mitogenic response and inadequate IL-2 production (p < 0.05-0.01) but did not affect the abnormal ratio of CD4 to CD8 T lymphocytes in blood (p > 0.05).
  
  
  CONCLUSIONS
  These results suggest that bacteria/endotoxin translocation from the gut appears to be involved in cell-mediated immune dysfunction as a consequence of thermal injury. Pretreatment with SDD might attenuate postburn immunosuppression by preventing translocation events.
authors.affiliation: Trauma Research Center, Postgraduate Medical College, 304th Hospital, Beijing, People's Republic of China.
authors.forename: Y M
authors.initials: YM
authors.lastname: Yao
authors.forename: L R
authors.initials: LR
authors.lastname: Lu
authors.forename: Y
authors.initials: Y
authors.lastname: Yu
authors.forename: H P
authors.initials: HP
authors.lastname: Liang
authors.forename: J S
authors.initials: JS
authors.lastname: Chen
authors.forename: Z G
authors.initials: ZG
authors.lastname: Shi
authors.forename: B T
authors.initials: BT
authors.lastname: Zhou
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Sheng
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D018988:Bacterial Translocation; D002056:Burns / Q000276:immunology* / Q000382:microbiology*; D002455:Cell Division; D002478:Cells, Cultured; D003091:Colistin / Q000627:therapeutic use; D004064:Digestive System / Q000276:immunology / Q000382:microbiology*; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood*; D005437:Flucytosine / Q000627:therapeutic use; D007111:Immunity, Cellular; D007165:Immunosuppression Therapy; D007376:Interleukin-2 / Q000096:biosynthesis; D007422:Intestines / Q000276:immunology / Q000382:microbiology; D016131:Lymphocyte Subsets / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000166:cytology; D014031:Tobramycin / Q000627:therapeutic use
chemical_list: D000900:Anti-Bacterial Agents; D004731:Endotoxins; D007376:Interleukin-2; D005437:Flucytosine; D014031:Tobramycin; D003091:Colistin