title: Effect of acute ethanol exposure on the dermal inflammatory response after burn injury.
abstract: BACKGROUND
  More than 100,000 people each year are admitted to U.S. hospitals for severe burn injury. Strikingly, ethanol use prior to injury is apparent in nearly 50% of burn patients, rendering them six times more likely to die from infection than patients not exposed to ethanol. We previously reported that the kinetics and magnitude of neutrophil chemokine production and subsequent accumulation of neutrophils in the lung was dramatically altered when ethanol exposure preceded injury. Here, we tested whether burn injury and ethanol exposure combined, altered susceptibility to infection, neutrophil chemoattractant production, and neutrophil accumulation at the site of the burn wound.
  
  
  METHODS
  Male B(6)D(2)F1 mice were administered a dose of ethanol designed to achieve 90-100 mg/dl circulating levels and 30 min later subjected to a 15% total body surface area dorsal scald injury. Susceptibility to topically applied Pseudomonas aeruginosa was examined. At various times after injury, burn wound and normal tissues were collected for assessments of neutrophil counts, myeloperoxidase quantitation, and neutrophil chemoattractant (KC and MIP-2) production.
  
  
  RESULTS
  Ethanol exposure prior to burn injury enhanced susceptibility to infection after burn and was associated with significantly elevated production of KC, but not MIP-2, at the wound site. Despite the enhanced elevation of KC, neutrophil accumulation in the wounds of ethanol exposed, burn injured mice did not differ from those that received burn injury alone. TNFalpha (a potent activator of neutrophils), however, was found to be significantly elevated in the wounds of mice that received only burn injury, but not in those that received injury in combination with prior ethanol exposure.
  
  
  CONCLUSIONS
  In the presence of ethanol, neutrophils are adequately recruited to the site of burn injury, but their host defense functions are impaired, perhaps due to the lack of proinflammatory cytokines such as TNFalpha.
authors.affiliation: Alcohol Research Program, Loyola University of Chicago, Maywood, IL 60153, USA. dfaunce@lumc.edu
authors.forename: Douglas E
authors.initials: DE
authors.lastname: Faunce
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Garner
authors.forename: Julian N
authors.initials: JN
authors.lastname: Llanas
authors.forename: Parag J
authors.initials: PJ
authors.lastname: Patel
authors.forename: Meredith S
authors.initials: MS
authors.lastname: Gregory
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Duffner
authors.forename: Richard L
authors.initials: RL
authors.lastname: Gamelli
authors.forename: Elizabeth J
authors.initials: EJ
authors.lastname: Kovacs
mesh_terms: D000818:Animals; D002056:Burns / Q000276:immunology / Q000382:microbiology / Q000401:mortality / Q000473:pathology*; D000431:Ethanol / Q000008:administration & dosage*; D007249:Inflammation / Q000209:etiology / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D008297:Male; D051379:Mice; D020556:Neutrophil Infiltration / Q000187:drug effects; D011552:Pseudomonas Infections / Q000401:mortality / Q000473:pathology; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000502:physiology
chemical_list: D014409:Tumor Necrosis Factor-alpha; D000431:Ethanol