title: Expression and significance of ICAM-1 and its counter receptors LFA-1 and Mac-1 in experimental acute pancreatitis of rats.
abstract: OBJECTIVE
  To investigate the role of intercellular adhesion molecule-1 (ICAM-1) and its counter receptors LFA-1 and Mac-1 in acute pancreatitis (AP).
  
  
  METHODS
  SD rats were allocated to AP group and control group randomly (25 rats each). AP was induced by infusion of 5% chenodeoxycholic acid into the pancreatic duct, followed by ligation of pancreatic duct. The rats were sacrificed at 1, 3, 6, 12 and 24 h after induction of pancreatitis. Five rats were sacrificed at one time point in the two groups before the blood and specimens from pancreas and lung were obtained. Serum amylase and ascitic fluid were measured at each time point. Expression of ICAM-1 at different time points was assessed by immunohistochemistry in pancreas and lung, and the expression of LAF-1 and Mac-1 on neutrophils at different time points was detected by flow cytometer.
  
  
  RESULTS
  Induction of AP was confirmed by the serum levels of amylase and histological studies. The expression of ICAM-1 in pancreas increased significantly than that in the control group at all time points (P<0.05 or P<0.01), as well as the expression in lung except at 1 h. The expression of LFA-1 and Mac-1 on neutrophil in blood increased significantly in AP group than that in control group at several time points (P<0.05 or P<0.01). The amount of ascitic fluid and serum amylase level of AP group increased significantly than that of control group at all time points (P<0.05 or P<0.01). Parallel to these results, a significant neutrophil infiltration was found in pancreas and lung tissues of AP group rats.
  
  
  CONCLUSIONS
  Our findings suggest the important role for ICAM-1, LFA-1 and Mac-1 in mediating the development of AP from a local disease to a systemic illness. Upregulation of ICAM-1, LFA-1, Mac-1 and subsequent leukocyte infiltration appear to be significant events of pancreatic and pulmonary injuries in AP.
authors.affiliation: Department of Pediatric Surgery, Kagawa Medical University, Japan. sunweii@hotmail.com
authors.forename: Wei
authors.initials: W
authors.lastname: Sun
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Watanabe
authors.forename: Zhong-Qiu
authors.initials: ZQ
authors.lastname: Wang
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood / Q000378:metabolism; D000818:Animals; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis* / Q000502:physiology*; D007962:Leukocytes / Q000378:metabolism; D008168:Lung / Q000473:pathology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis*; D016177:Macrophage-1 Antigen / Q000096:biosynthesis*; D009504:Neutrophils / Q000378:metabolism; D010179:Pancreas / Q000378:metabolism; D010195:Pancreatitis / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D018799:Intercellular Adhesion Molecule-1; D000681:Amylases