PGE2 suppresses intestinal T cell function in thermal injury: a cause of enhanced bacterial translocation

Shock. 2001 Sep;16(3):183-8. doi: 10.1097/00024382-200116030-00003.


Increased gut bacterial translocation in burn and trauma patients has been demonstrated in a number of previous studies, however, the mechanism for such an increased gut bacterial translocation in injured patients remains poorly understood. Utilizing a rat model of burn injury, in the present study we examined the role of intestinal immune defense by analyzing the T cell functions. We investigated if intestinal T cells dysfunction contributes to bacterial translocation after burn injury. Also our study determined if burn-mediated alterations in intestinal T cell functions are related to enhanced release of PGE2. Finally, we examined whether or not burn-related alterations in intestinal T cell function are due to inappropriate activation of signaling molecule P59fyn, which is required for T cell activation and proliferation. The results presented here showed an increase in gut bacterial accumulation in mesenteric lymph nodes after thermal injury. This was accompanied by a decrease in the intestinal T cell proliferative responses. Furthermore, the treatments of burn-injured animals with PGE2 synthesis blocker (indomethacin or NS398) prevented both the decrease in intestinal T cell proliferation and enhanced bacterial translocation. Finally, our data suggested that the inhibition of intestinal T cell proliferation could result via PGE2-mediated down-regulation of the T cell activation-signaling molecule P59fyn. These findings support a role of T cell-mediated immune defense against bacterial translocation in burn injury.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bacterial Translocation / drug effects
  • Bacterial Translocation / physiology*
  • Burns / complications
  • Burns / microbiology
  • Burns / physiopathology*
  • Cyclooxygenase Inhibitors / pharmacology
  • Dinoprostone / metabolism*
  • Indomethacin / pharmacology
  • Intestines / drug effects
  • Intestines / immunology*
  • Intestines / physiopathology
  • Lymph Nodes / cytology
  • Lymph Nodes / microbiology
  • Male
  • Nitrobenzenes / pharmacology
  • Phosphorylation
  • Proto-Oncogene Proteins / drug effects
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-fyn
  • Rats
  • Rats, Sprague-Dawley
  • Sulfonamides / pharmacology
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / physiology*


  • Cyclooxygenase Inhibitors
  • Nitrobenzenes
  • Proto-Oncogene Proteins
  • Sulfonamides
  • N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
  • Fyn protein, rat
  • Proto-Oncogene Proteins c-fyn
  • Dinoprostone
  • Indomethacin