title: [A low level of TNF-mediates hemorrhage-induced acute lung injury via p55 TNF receptor].
abstract: OBJECTIVE
  To examine the temporal relationship of pulmonary TNF-alpha production to acute lung injury (ALI) during hemorrhagic shock (HS).
  
  
  METHODS
  HS was induced in mice by removal of 30% of calculated total blood volume. Lung TNF-alpha was measured by ELISA. Lung neutrophil accumulation was detected by immunofluorescent staining, and pulmonary microvascular permeability was assessed using Evans blue dye.
  
  
  RESULTS
  While HS induced a slight and transient increase in lung TNF-alpha, neutrophil accumulation preceded the change in lung TNF-alpha. However, lung neutrophil accumulation and the increase in microvascular permeability were abrogated in TNF-alpha knockout mice, and both were restored by administration of low dose TNF-alpha to TNF-alpha knockout mice prior to HS. Both neutrophil accumulation and microvascular leak were abrogated in p55 TNF-alpha receptor knockout mice, while p75 TNF-alpha receptor knockout mice behaved similar to wild type.
  
  
  CONCLUSIONS
  A low level of pulmonary TNF-alpha is sufficient to mediate HS-induced acute lung injury and that the p55 TNF-alpha receptor plays a dominant role in regulating the pulmonary inflammatory response to HS. The results suggest that anti-TNF-alpha strategies for the control of the pulmonary inflammatory response to HS can be directed toward antagonizing the p55 TNF-alpha receptor.
authors.affiliation: Department of Respiratory Medicine, Nanjing General Hospital of PLA, Nanjing 210002, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Song
authors.forename: Yi
authors.initials: Y
authors.lastname: Shi
authors.forename: Alden H
authors.initials: AH
authors.lastname: Harken
authors.forename: Xianzhong
authors.initials: X
authors.lastname: Meng
authors.forename: Christopher D
authors.initials: CD
authors.lastname: Raeburn
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology*; D047888:Receptors, Tumor Necrosis Factor, Type I; D012128:Respiratory Distress Syndrome / Q000209:etiology*; D012771:Shock, Hemorrhagic / Q000150:complications*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: D015703:Antigens, CD; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha