[Influence of stress inhibition on invasive infection in burn wound during early postburn stage in severely burned rats]

Zhonghua Shao Shang Za Zhi. 2005 Apr;21(2):85-8.
[Article in Chinese]

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).

Conclusion: 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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Burns / metabolism
  • Burns / microbiology*
  • Disease Models, Animal
  • Interferon-gamma / metabolism
  • Interleukin-10 / metabolism
  • Interleukin-2 / metabolism
  • Interleukin-4 / metabolism
  • Pseudomonas Infections / immunology*
  • Rats
  • Rats, Sprague-Dawley
  • Th1 Cells / metabolism
  • Th2 Cells / metabolism
  • Wound Infection / therapy*

Substances

  • Interleukin-2
  • Interleukin-10
  • Interleukin-4
  • Interferon-gamma