title: Smoke inhalation enhances early alveolar leukocyte responsiveness to endotoxin.
abstract: BACKGROUND
  Pulmonary dysfunction after smoke inhalation and thermal injury is associated with excessive morbidity and mortality. The purpose of this study was to evaluate alveolar leukocyte function after thermal injury and smoke inhalation.
  
  
  METHODS
  Twenty-one patients with thermal injury only (n = 8); thermal injury and smoke inhalation injury (n = 8); and nonburned controls (n = 5) were assessed by means of bronchoscopically directed lavage (bronchoalveolar lavage [BAL]) on the first and fourth days postinjury. BAL-isolated pulmonary leukocytes were assessed for number, composition, viability, and production of tumor necrosis factor (TNF)alpha, interleukin (IL)-8, and IL-6 in response to 100 ng/mL of lipopolysaccharide (LPS) (mean +/- SEM; significance at p < 0.05).
  
  
  RESULTS
  Six of eight Smoke patients had gross evidence of lung injury. On day 1, Smoke and Burn BAL isolates yielded greater cell counts than Control (10.6 vs. 4.5 vs. 2.4 x 10(6)/mL). Smoke macrophages on day 1 produced more TNFalpha (1.2 vs. 0.2 ng/mL), IL-6 (8.0 vs. 1.9 ng/mL), and IL-8 (85 vs. 32 ng/mL) after LPS stimulation compared with respective unstimulated (0 ng/mL of LPS) day-1 Smoke cells. LPS-stimulated Burn cells on day 1 produced more IL-8 (150 vs. 62 ng/mL) but not TNFalpha (0.4 vs. 0.25 ng/mL) or IL-6 (1.8 vs. 0.69 ng/mL), when compared with respective unstimulated Burn cells. By day 4, LPS-stimulated Smoke and Burn cells produced significantly more TNFalpha (Smoke, 0.41 vs. 0.16 ng/mL; Burn, 0.87 vs. 0.51 ng/mL) and IL-6 (Smoke, 2.5 vs. 0.47 ng/mL; Burn, 4.1 vs. 1.47 ng/mL), but not IL-8 (Smoke, 51.1 vs. 51.1 ng/mL; Burn, 54.4 vs. 55.6 ng/mL), compared with respective unstimulated day-4 cells.
  
  
  CONCLUSIONS
  Smoke inhalation induces a massive influx of alveolar leukocytes that are primed for an early, enhanced LPS-activated cytokine response compared with alveolar leukocytes isolated after burn injury alone or normal controls.
authors.affiliation: Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390-9158, USA.
authors.forename: Mary Jo
authors.initials: MJ
authors.lastname: Wright
authors.forename: Joseph T
authors.initials: JT
authors.lastname: Murphy
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D018893:Bronchoalveolar Lavage; D001999:Bronchoscopy; D002056:Burns / Q000378:metabolism*; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis / Q000378:metabolism; D016209:Interleukin-8 / Q000096:biosynthesis / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D016676:Macrophages, Alveolar / Q000378:metabolism*; D008297:Male; D015208:Smoke Inhalation Injury / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha