title: Serum levels of Hsp60 correlate with the development of acute lung injury after trauma.
abstract: BACKGROUND
  Previous studies have shown that heat shock protein 60 (Hsp60) is a danger signal for the immune system and appears to be a key endogenous inflammatory mediator that activates the toll-like receptors and causes the release of proinflammatory cytokines and nitric oxide by immune competent cells, but no data are available for trauma patients. The purpose of this study was to determine whether Hsp60 could be detected in the serum of patients early after severe trauma and whether its serum level might correlate with the development of acute lung injury (ALI) in trauma patients.
  
  
  METHODS
  Clinical data were collected prospectively during a 12-month period for trauma patients who were ventilated mechanically for more than 24 h and who met the following inclusion criteria: Injury Severity Score > or =16, age >18 years. Physiological data for quantitative assessment of organ dysfunction were collected for each patient. Hsp60 levels were measured in the serum of trauma patients.
  
  
  RESULTS
  Sixty-four patients with severe trauma were enrolled in the study. Eighteen patients developed ALI (28%). Trauma patients who later developed ALI had significantly higher serum values of Hsp60 than those who did not (4.21 +/- 2.24 ng/mL versus 0.73 +/- 0.26 ng/mL, P < 0.05, mean +/- SE). Furthermore, immature but not mature recombinant Hsp60 induced in vitro the release of nitric oxide (NO) from RAW 264.7 murine macrophages.
  
  
  CONCLUSIONS
  Serum levels of Hsp60 detected within 30 min after trauma correlate with the development of ALI. Immature but mature Hsp60 causes in vitro the release of NO by macrophages, suggesting that the extracellular release of the immature Hsp60 associated with traumatic cell necrosis could be involved in the release of NO by immune competent cells, leading to an activation of the inflammatory response within the lung or other organs.
authors.affiliation: Department of Anesthesia, San Francisco General Hospital, University of California, California 94110, USA.
authors.forename: Melissa
authors.initials: M
authors.lastname: Pespeni
authors.forename: Robert C
authors.initials: RC
authors.lastname: Mackersie
authors.forename: Hyon
authors.initials: H
authors.lastname: Lee
authors.forename: Diane
authors.initials: D
authors.lastname: Morabito
authors.forename: Maki
authors.initials: M
authors.lastname: Hodnett
authors.forename: Marybeth
authors.initials: M
authors.lastname: Howard
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Pittet
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D018834:Chaperonin 60 / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D008875:Middle Aged; D009569:Nitric Oxide / Q000096:biosynthesis; D009573:Nitrites / Q000378:metabolism; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000097:blood*; D014947:Wounds and Injuries / Q000097:blood* / Q000150:complications
chemical_list: D018834:Chaperonin 60; D009573:Nitrites; D009569:Nitric Oxide