title: Expression of the chemokines MCP-1/JE and cytokine-induced neutrophil chemoattractant in early acute pancreatitis.
abstract: BACKGROUND
  Inflammatory mediators play a critical role in acute pancreatitis. The precise role played by members of the chemokine family remains unclear.
  
  
  OBJECTIVE
  To investigate the expression of the CC chemokine monocyte chemotactic protein (MCP)-1/JE and the CXC chemokine cytokine-induced neutrophil chemoattractant (CINC) in early acute pancreatitis.
  
  
  METHODS
  Pancreatitis was induced in rats, either by intraperitoneal injection of cerulein or by infusion of 5% sodium taurocholate into the pancreatic duct. Expression of MCP-1/JE and CINC in pancreas and plasma was determined by immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), Northern analysis, and quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  Following induction of acute pancreatitis, MCP-1/JE and CINC immunoreactivity was seen in acinar cells. Infiltrating neutrophils were strongly immunolabeled with an anti-MCP-1/JE antibody, whereas macrophages reacted strongly with an antibody to CINC. Northern analysis and quantitative real-time RT-PCR demonstrated upregulation of MCP-1/JE and CINC mRNA levels in pancreatic tissue. Plasma MCP-1 levels were significantly increased after 6 hours in the cerulein hyperstimulation model (2,444 +/- 93 microg/mL versus control, 1,853 +/- 262 microg/mL; < 0.05). Plasma CINC levels were significantly increased after 6 hours in the cerulein hyperstimulation model (1,680 +/- 134 microg/mL versus control, 725 +/- 128 microg/mL; < 0.005) and after 3 hours in the bile salt infusion model (6,663 +/- 1,405 microg/mL versus control, 2,339 +/- 800 microg/mL; < 0.05).
  
  
  CONCLUSIONS
  CINC and MCP-1/JE may be early mediators of the inflammatory response in acute pancreatitis.
authors.affiliation: Department of Surgery, University of Liverpool and Royal Liverpool University Hospital, Liverpool, United Kingdom.
authors.forename: Mark
authors.initials: M
authors.lastname: Brady
authors.forename: Madhav
authors.initials: M
authors.lastname: Bhatia
authors.forename: Stephen
authors.initials: S
authors.lastname: Christmas
authors.forename: Mark T
authors.initials: MT
authors.lastname: Boyd
authors.forename: John P
authors.initials: JP
authors.lastname: Neoptolemos
authors.forename: John
authors.initials: J
authors.lastname: Slavin
mesh_terms: D000208:Acute Disease; D000818:Animals; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D018925:Chemokines / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008297:Male; D010195:Pancreatitis / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014158:Transcription, Genetic
chemical_list: D018932:Chemokine CCL2; D018925:Chemokines; D019743:Chemokines, CXC; D002630:Chemotactic Factors; D036341:Intercellular Signaling Peptides and Proteins; D012333:RNA, Messenger