title: [Influence of stress inhibition on invasive infection in burn wound during early postburn stage in severely burned rats].
abstract: OBJECTIVE
  To investigate the influence of inhibition of stress on the survival rate, organ dysfunction and (Th)1/Th2 cytokine profiles of the rats with invasive infection in the wound at early postburn stage.
  
  
  METHODS
  Sprague-Dawley rats inflicted with 30% TBSA full thickness burn were randomly divided into A (n = 36, with immediate resuscitation), B (n = 36, with immediate resuscitation and lytic cocktail administration). After subeschar injection of 0.1 ml Pseudomonas aeruginosa (10(8) CFU/ml) on 3rd postburn day, the subeschar bacterial quantitative analysis, the survival rate at 96 hours after bacteria injection, the parameters of organ dysfunction and the mRNA expression of IL-2, IL-4, IL-10 and IFN-gamma were determined by corresponding methods.
  
  
  RESULTS
  The quantity of subeschar bacteria was larger than 1 x 10(5)/gram in both groups. The survival rate in B group (66.7 +/- 2.6)% was obviously higher than that in A group (33.3 +/- 1.7)%, (P < 0.01). Inflammatory infiltration and pathological changes in the internal organs in B group were alleviated obviously compared with A group. The expression of IL-2 mRNA in B group was significantly lower than that in A group before bacterial inoculation, but increased at 48 and 96 hours after bacterial inoculation, while it was lowered in A group at the same time points (P < 0.05). The expression of IFN-gamma mRNA in A group was significantly lower than that in B group (P < 0.01), while that of IL-4 and IL-10 mRNA in A group was evidently higher than that in B group (P < 0.05 approximately 0.01).
  
  
  CONCLUSIONS
  Inhibition of the stress response during early postburn stage could be beneficial to the prevention of the bacterial invasion due to the changes in Th1/Th2 ratio.
authors.affiliation: Department of Burns, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, P.R. China.
authors.forename: Liang
authors.initials: L
authors.lastname: Qiao
authors.forename: Hui-zhong
authors.initials: HZ
authors.lastname: Yang
authors.forename: Ke-jian
authors.initials: KJ
authors.lastname: Yuan
authors.forename: Wen-kui
authors.initials: WK
authors.lastname: Wang
authors.forename: He-liang
authors.initials: HL
authors.lastname: Dong
authors.forename: Wei-shi
authors.initials: WS
authors.lastname: Xu
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism / Q000382:microbiology*; D004195:Disease Models, Animal; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D011552:Pseudomonas Infections / Q000276:immunology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism; D014946:Wound Infection / Q000628:therapy*
chemical_list: D007376:Interleukin-2; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma