title: Mesenteric lymph from burned rats induces endothelial cell injury and activates neutrophils.
abstract: OBJECTIVE
  Our previous studies indicated that mesenteric lymph duct ligation prevented burn-induced lung injury. Thus, the goal of the present study was to begin to investigate potential mechanisms of this protective effect.
  
  
  METHODS
  Prospective animal study with concurrent control.
  
  
  METHODS
  Small animal laboratory.
  
  
  METHODS
  Adult male Sprague-Dawley rats.
  
  
  METHODS
  Mesenteric lymph and portal vein plasma were collected from male rats subjected to a 40% third-degree scald burn or sham burn. The biological effects of these lymph and plasma samples were tested for their ability to kill human umbilical vein endothelial cells (HUVECs), increase HUVEC monolayer permeability, and activate polymorphonuclear leukocytes (PMNs), as reflected in CD11b adhesion molecule expression and superoxide production. Additionally, ileal specimens were harvested at the end of the experiment (6 hrs postburn) for histologic analysis.
  
  
  RESULTS
  Postburn mesenteric lymph produced during the first 2 hrs after burn injury and tested at a 5% concentration, but not sham-burn lymph or portal plasma from burned rats, was toxic for HUVECs resulting in cell death after an 18-hr incubation period. Similarly, only postburn lymph increased HUVEC monolayer permeability. Postburn lymph activated both rat and human PMNs as reflected in increased CD11b expression and augmentation of the phorbol myristate acetate-induced superoxide response. Neither sham-burn lymph nor postburn portal vein plasma activated PMNs. Both the burn and sham-burn lymph samples were sterile, indicating that the effects of burn lymph on the HUVECs or PMNs were not due to translocating bacteria. Last, an association was found between burn-induced gut injury and the production of toxic burn lymph.
  
  
  CONCLUSIONS
  Burn-induced gut injury results in the production of biologically active factors that are carried in the mesenteric lymph, but not the portal plasma, which injure endothelial cells and activate PMNs and thus could contribute to distant organ injury.
authors.affiliation: Department of Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07101, USA. edeitech@umdnj.edu
authors.forename: Edwin A
authors.initials: EA
authors.lastname: Deitch
authors.forename: Han Ping
authors.initials: HP
authors.lastname: Shi
authors.forename: Qi
authors.initials: Q
authors.lastname: Lu
authors.forename: Eleonora
authors.initials: E
authors.lastname: Feketeova
authors.forename: Joan
authors.initials: J
authors.lastname: Skurnick
authors.forename: Da Zhong
authors.initials: DZ
authors.lastname: Xu
mesh_terms: D000818:Animals; D002056:Burns / Q000276:immunology*; D003602:Cytotoxicity, Immunologic; D004730:Endothelium, Vascular / Q000166:cytology* / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology*; D008297:Male; D008643:Mesentery; D018375:Neutrophil Activation; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley