title: Early but not late burn wound excision partially restores viral-specific T lymphocyte cytotoxicity.
abstract: OBJECTIVE
  Early burn wound excision restores immunocompetence and improves patient survival, but the exact mechanisms have not yet been defined. Burn injury impairs cytotoxic T lymphocyte (CTL) activity as a function of burn size, increasing the risk of infection. The purpose of this study was to determine if early wound excision improved viral-specific CTL function.
  
  
  METHODS
  Anesthetized C57BL/6 mice (n = 20) received 0%, 20%, or 40% total body surface area full-thickness contact burns and were inoculated 3 days later with intraperitoneal lymphocytic choriomeningitis virus. Eight days after infection, or 11 days after burn, CTL effectors (E) were harvested and tested against infected, radiolabeled L-Dh targets (T) in a 51Cr-release assay, at varied E:T ratios. Dilution curves of CTL activity were compared by analysis of variance. In the second experiment, mice (n = 18) underwent a 30% burn that was totally excised and grafted on postburn days (PBDs) 0, 3, and 7. Control groups included sham burn and no excision of a 30% burn. In the third experiment, mice (n = 22) received a 30% burn that was partially, completely, or not excised on PBD 3. Control groups included sham burn with and without excision. All groups were infected with intraperitoneal lymphocytic choriomeningitis virus on PBD 3. Viral-specific CTL activity was determined on PBD 11.
  
  
  RESULTS
  Both 20% and 40% burn injury impaired viral-specific CTL function. Wound excision on PBDs 0 and 3, but not on PBD 7, partially restored CTL function. Total excision of the 30% burn improved CTL activity to a greater extent than did partial excision.
  
  
  CONCLUSIONS
  Burn injury inhibits viral-specific CTL activity. Early, complete wound excision augments CTL function. Improved CTL activity after burn may reduce the risk of infection, providing an immunologic rationale for expeditious wound excision.
authors.affiliation: Department of Surgery, University of North Carolina, Chapel Hill 27599-7210, USA.
authors.forename: C S
authors.initials: CS
authors.lastname: Hultman
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: S
authors.initials: S
authors.lastname: deSerres
authors.forename: J A
authors.initials: JA
authors.lastname: Frelinger
authors.forename: A A
authors.initials: AA
authors.lastname: Meyer
mesh_terms: D000818:Animals; D002056:Burns / Q000276:immunology* / Q000601:surgery* / Q000821:virology; D005260:Female; D008217:Lymphocytic choriomeningitis virus / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D013997:Time Factors