title: Pulmonary LPS-binding protein (LBP) upregulation following LPS-mediated injury.
abstract: BACKGROUND
  The acute respiratory distress syndrome (ARDS) causes significant morbidity and mortality among trauma patients. Although multiple factors have been implicated, pulmonary injury in this population may be due to inflammatory mediators released in response to stimuli such as endotoxin (LPS). LBP plays an integral part in LPS-mediated release of inflammatory cytokines and increased local expression of LBP as the result of a primary injury may prime the lung to secondary LPS-mediated damage.
  
  
  METHODS
  To determine the magnitude of pulmonary LBP upregulation following LPS injury we challenged rats with either intravenous (IV) or intratracheal (IT) LPS. Animals from each group were euthanized at 1, 2, 4, and 8 h postchallenge. Lung LBP and CD14 mRNA levels were assayed by Northern blot. Serum and bronchoalveolar lavage (BAL) fluid were assayed for inflammatory cytokines (TNF-alpha, MCP-1, IL-1beta, IL-6, and IL-10) by ELISA.
  
  
  RESULTS
  LBP and CD14 mRNA levels were found to increase significantly in lung tissue after both IV and IT LPS with the IV LPS animals having a greater increase over 8 h. Serum TNF-alpha was significantly elevated in the IV LPS group whereas very low levels were detected in the BAL. Only BAL TNF-alpha was increased in the IT group at 8 h.
  
  
  CONCLUSIONS
  Local pulmonary LBP and CD14 mRNA are both upregulated after either systemic or local LPS exposure. Such upregulation may render thelung more susceptible to local immune overactivation and injury during subsequent exposures to LPS.
authors.affiliation: Department of Surgery, University of Michigan, Ann-Arbor, Michigan 48109, USA.
authors.forename: R D
authors.initials: RD
authors.lastname: Klein
authors.forename: G L
authors.initials: GL
authors.lastname: Su
authors.forename: A
authors.initials: A
authors.lastname: Aminlari
authors.forename: W H
authors.initials: WH
authors.lastname: Alarcon
authors.forename: S C
authors.initials: SC
authors.lastname: Wang
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000378:metabolism; D015870:Gene Expression / Q000502:physiology; D007375:Interleukin-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D008562:Membrane Glycoproteins; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D018932:Chemokine CCL2; D007375:Interleukin-1; D016753:Interleukin-10; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein