title: Occult injury in the residual lung after pneumonectomy in mice.
abstract: OBJECTIVE
  We aimed to determine the acute phase impact of pneumonectomy with respect to injury in the remaining lung using a murine model, and to investigate the profiles of inflammatory mediators including high mobility group box 1 protein (HMGB1) following surgery and administration of low dose intratracheal lipopolysaccharide.
  
  
  METHODS
  Mice received left pneumonectomy with intratracheal administration of either saline or lipopolysaccharide. Lung permeability index, lung wet-to-dry weight ratio, pathological findings, HMGB1 levels in bronchoalveolar lavage fluid (BALF) and plasma, and cytokine profiles in BALF were assessed 24 h after surgery.
  
  
  RESULTS
  Index of capillary permeability, lung water content, and neutrophil and macrophage counts in BALF were significantly increased by pneumonectomy. These parameters were highest in the mice with pneumonectomy with intratracheal administration of lipopolysaccharide. On lung pathology, neutrophil infiltration was prominent in the residual lung after pneumonectomy. HMGB1 levels were significantly higher in both BALF and plasma in the mice with pneumonectomy, and were highest in those with pneumonectomy and intratracheal administration of lipopolysaccharide. Pro-inflammatory cytokine levels including interferon-gamma significantly increased in BALF in the mice with pneumonectomy.
  
  
  CONCLUSIONS
  It was suggested that pneumonectomy itself may cause occult lung injury in the acute phase (24 h) of post-surgery which could be enhanced by inflammatory stimulus, such as bacterial component, leading to significant lung injury. HMGB1 might be involved in the pathogenesis of the occult lung injury.
authors: Department of Surgery, Saiseikai Utsunomiya Hospital, Tochigi, Japan.
authors: Atsushi
authors: A
authors: Tajima
authors: Mitsutomo
authors: M
authors: Kohno
authors: Masazumi
authors: M
authors: Watanabe
authors: Yotaro
authors: Y
authors: Izumi
authors: Sadatomo
authors: S
authors: Tasaka
authors: Ikuro
authors: I
authors: Maruyama
authors: Taku
authors: T
authors: Miyasho
authors: Koichi
authors: K
authors: Kobayashi
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002199:Capillary Permeability; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D024243:HMGB1 Protein / Q000097:blood / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008168:Lung / Q000098:blood supply / Q000276:immunology / Q000473:pathology / Q000601:surgery*; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000473:pathology; D009929:Organ Size; D011013:Pneumonectomy / Q000009:adverse effects*; D011654:Pulmonary Edema / Q000209:etiology; D012720:Severity of Illness Index; D013997:Time Factors; D055114:X-Ray Microtomography
chemical_list: D016207:Cytokines; D024243:HMGB1 Protein; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; C482199:lipopolysaccharide, E coli O55-B5