title: Expression and function of endothelial monocyte-activating polypeptide-II in acute lung inflammation.
abstract: OBJECTIVE
  We tested the hypothesis that total endothelial monocyte-activating polypeptide-II (EMAP-II) expression (proEMAP/p43 and mature EMAP-II) is up-regulated in lipopolysaccharide (LPS)-induced acute lung inflammation (ALI) and that mature EMAP-II induces monocyte/macrophage and granulocyte recruitment in vivo.
  
  
  METHODS
  Thirty-five 10 week old, male Sprague-Dawley rats.
  
  
  METHODS
  Animals were instilled intratracheally with 250 microg of E. coli LPS (N = 15) or saline (N = 5) or 20 microg of mature EMAP-II (N = 5).
  
  
  METHODS
  Total EMAP-II was quantified using ELISA and the protein was localized with light and electron microscopic immunocytochemistry in lungs of rats at 1, 3 and 12 h (n = 5/group).
  
  
  RESULTS
  ELISA showed increased total EMAP-II concentrations (p < 0.05) in lungs from LPS-treated rats compared to control animals. Compared to the controls, light and electron microscopic imunocytochemistry localized total EMAP-II in monocytes/macrophages and alveolar septa at 1 and 3 h and in vascular smooth muscles at 12 h post-LPS treatment. Instillation of mature EMAP-II increased lung monocytes/macrophages and granulocytes compared with control animals (p < 0.05). However, compared to the LPS treatment, mature EMAP-II instillation did not induce expression of IL-1beta and MIP-2 (p < 0.05) and provoked less vigorous recruitment of monocytes/macrophages.
  
  
  CONCLUSIONS
  EMAP-II expression is increased in LPS-induced ALI, and that intra-tracheal instillation of mature EMAP-II induces recruitment of monocytes/macrophages and granulocytes into the lungs without stimulating IL-1beta or MIP-2 expression.
authors: Immunology Research Group, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada, S7N 5B4.
authors: W Shane
authors: WS
authors: Journeay
authors: K S
authors: KS
authors: Janardhan
authors: B
authors: B
authors: Singh
mesh_terms: D000208:Acute Disease; D000818:Animals; D054426:Chemokine CXCL2; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006098:Granulocytes / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides; D008168:Lung / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D008264:Macrophages / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D015846:Monokines / Q000235:genetics / Q000378:metabolism; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D011014:Pneumonia / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D016601:RNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D054426:Chemokine CXCL2; D016207:Cytokines; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D015846:Monokines; D009363:Neoplasm Proteins; D016601:RNA-Binding Proteins; C077219:small inducible cytokine subfamily E, member 1