title: Differential expression of chemokines in normal pancreas and in chronic pancreatitis.
abstract: OBJECTIVE
  Cellular infiltrates are present already in early stages of chronic pancreatitis. The mechanisms responsible for their recruitment are unknown. Hence, we determined the differential expression of chemokine genes and their cellular sources in normal and affected pancreatic tissues.
  
  
  METHODS
  Pancreatic tissues from 23 patients with chronic pancreatitis and from 4 normal controls were subjected to in situ hybridization for detecting messenger RNA (mRNA) of the chemokine genes interleukin 8, ENA-78, MIG, MCP-1, and I-309.
  
  
  RESULTS
  Normal pancreatic tissues lack cells expressing mRNA for IL-8, ENA-78, MIG, and MCP-1. In contrast, pancreatic lobuli with mild to moderate signs of tissue alterations strongly expressed MCP-1 mRNA in centroacinar ducts, endothelia, fibroblasts, macrophages, T cells, and occasionally in nerves. Interleukin 8 and ENA-78 mRNA is preferentially detected in centroacinar ducts of pancreatic lobuli with more advanced alterations. Variable numbers of pancreas-infiltrating T cells express MIG mRNA. I-309 mRNA, however, is consistently observed in normal acini and in tissue with mild to moderate signs of tissue alterations.
  
  
  CONCLUSIONS
  The observed differential expression of distinct chemokine genes in pancreatic parenchyma and infiltrates from patients with chronic pancreatitis strongly suggests an involvement of distinct chemokines in the initiation and perpetuation of disease.
authors.affiliation: Department of Pathology, University of Bern, Bern, Switzerland.
authors.forename: L
authors.initials: L
authors.lastname: Saurer
authors.forename: P
authors.initials: P
authors.lastname: Reber
authors.forename: T
authors.initials: T
authors.lastname: Schaffner
authors.forename: M W
authors.initials: MW
authors.lastname: Büchler
authors.forename: C
authors.initials: C
authors.lastname: Buri
authors.forename: A
authors.initials: A
authors.lastname: Kappeler
authors.forename: A
authors.initials: A
authors.lastname: Walz
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: C
authors.initials: C
authors.lastname: Mueller
mesh_terms: D000328:Adult; D018932:Chemokine CCL2 / Q000235:genetics; D054365:Chemokine CXCL5; D054370:Chemokine CXCL9; D018925:Chemokines / Q000032:analysis* / Q000235:genetics*; D019743:Chemokines, CXC / Q000235:genetics; D002908:Chronic Disease; D005260:Female; D005355:Fibrosis; D006801:Humans; D007249:Inflammation; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8 / Q000031:analogs & derivatives / Q000235:genetics; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000276:immunology*; D010183:Pancreatic Ducts / Q000276:immunology / Q000473:pathology; D010195:Pancreatitis / Q000276:immunology* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: C486263:CXCL5 protein, human; C080810:CXCL9 protein, human; D018932:Chemokine CCL2; D054365:Chemokine CXCL5; D054370:Chemokine CXCL9; D018925:Chemokines; D019743:Chemokines, CXC; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8; D012333:RNA, Messenger