title: Chemokine gene expression in rat pancreatic acinar cells is an early event associated with acute pancreatitis.
abstract: OBJECTIVE
  The molecular mechanisms underlying pancreatitis are largely unknown. The goal of this study was to identify an early genetic event that correlated with pancreatitis.
  
  
  METHODS
  Differential display of messenger RNAs (mRNAs) was conducted on normal pancreas vs. those of animals with secretagogue-induced pancreatitis. Northern blots from normal animals and animals with experimental acute pancreatitis were probed with cloned complementary DNAs for chemokines. Pancreatitis was induced with cerulein and by retrograde injection of bile salts. Immunocytochemistry was used to identify the source of chemokine expression. Pyrrolidine dithiocarbamate was tested for effects on chemokine expression and pancreatitis.
  
  
  RESULTS
  A differentially amplified band was consistently observed early after cerulein hyperstimulation. This band was identified as a portion of the mob-1 gene, an alpha-chemokine. Northern analysis indicated that mRNAs for mob-1 and another chemokine, mcp-1, were induced after cerulein hyperstimulation in vivo. mob-1 mRNA was also induced by retrograde injection of bile salts and by cerulein in acinar cells in vitro. mob-1 protein was localized to exocrine cells in pancreata of diseased animals. Pyrrolidine dithiocarbamate inhibited both chemokine gene expression and early inflammatory characteristics of pancreatitis.
  
  
  CONCLUSIONS
  Chemokines are induced in acinar cells by treatments that induce pancreatitis and may play an important role in the early stages of the disease.
authors.affiliation: Department of Physiology, University of Michigan Medical School, Ann Arbor, USA.
authors.forename: T
authors.initials: T
authors.lastname: Grady
authors.forename: P
authors.initials: P
authors.lastname: Liang
authors.forename: S A
authors.initials: SA
authors.lastname: Ernst
authors.forename: C D
authors.initials: CD
authors.lastname: Logsdon
mesh_terms: D000208:Acute Disease; D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D054357:Chemokine CXCL10; D018925:Chemokines / Q000037:antagonists & inhibitors / Q000235:genetics*; D019743:Chemokines, CXC; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D015870:Gene Expression / Q000502:physiology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D010179:Pancreas / Q000473:pathology / Q000503:physiopathology*; D010195:Pancreatitis / Q000235:genetics* / Q000473:pathology; D011759:Pyrrolidines / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D013859:Thiocarbamates / Q000494:pharmacology; D013997:Time Factors
chemical_list: D018932:Chemokine CCL2; D054357:Chemokine CXCL10; D018925:Chemokines; D019743:Chemokines, CXC; C091326:Cxcl10 protein, rat; D016207:Cytokines; D016328:NF-kappa B; D011759:Pyrrolidines; D012333:RNA, Messenger; D013859:Thiocarbamates; C020972:pyrrolidine dithiocarbamic acid