title: Decreased expression of intestinal chemokine TECK/CCL25 in experimental obstructive jaundice and its reversal following internal biliary drainage.
abstract: BACKGROUND
  Although bacterial translocation is a significant problem in patients with obstructive jaundice, how translocation is promoted in this situation is not clearly understood. We previously reported the recovery of gut mucosal T-lymphocyte numbers in jaundiced rats following internal biliary drainage. This suggests that bile in the intestinal lumen promotes T-lymphocyte redistribution into the gut mucosa. To test this hypothesis, we have examined the expression patterns of chemokines that play an important role in lymphocyte recruitment into the small intestine.
  
  
  METHODS
  Four groups of rats receiving one of the following surgical procedures were studied: a sham operation (SHAM), common bile duct ligation (CBDL), CBDL followed by external drainage, or CBDL followed by internal drainage. Expression levels of intestinal mRNAs encoding TECK, MECK, and LARC chemokines were assessed using real-time polymerase chain reaction. Distribution of chemokine mRNA in the rat ileum was examined using in situ hybridization (ISH).
  
  
  RESULTS
  Following surgery, the expression levels of TECK mRNA decreased significantly in the CBDL group compared with in the SHAM group. While TECK expression did not recover after external drainage, it recovered to a near-normal level after internal drainage. Expression levels of MECK and LARC mRNAs were similar among all groups. ISH confirmed strong expression of TECK mRNA in the epithelial cells of the small intestine.
  
  
  CONCLUSIONS
  These results indicate that bile may contribute to high expression levels of TECK/CCL25 mRNA in the small intestine. Bile may also have a role in regulating the distribution of gut mucosal T lymphocytes by promoting TECK production from epithelial cells.
authors.affiliation: Department of Surgery, Division of Hepato-Biliary-Pancreatic Surgery, Kobe University Graduate School of Medical Sciences, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
authors.forename: Taku
authors.initials: T
authors.lastname: Matsumoto
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Ajiki
authors.forename: Eiji
authors.initials: E
authors.lastname: Kajiwara
authors.forename: Yoshiyasu
authors.initials: Y
authors.lastname: Mita
authors.forename: Tsunenori
authors.initials: T
authors.lastname: Fujita
authors.forename: Haruki
authors.initials: H
authors.lastname: Morimoto
authors.forename: Masaaki
authors.initials: M
authors.lastname: Miyazawa
authors.forename: Yonson
authors.initials: Y
authors.lastname: Ku
mesh_terms: D000818:Animals; D019742:Chemokines, CC / Q000096:biosynthesis / Q000235:genetics*; D003135:Common Bile Duct / Q000601:surgery*; D004195:Disease Models, Animal; D004322:Drainage / Q000379:methods*; D005786:Gene Expression Regulation; D007082:Ileum / Q000378:metabolism*; D017403:In Situ Hybridization; D041781:Jaundice, Obstructive / Q000235:genetics / Q000378:metabolism* / Q000601:surgery; D008026:Ligation / Q000009:adverse effects; D008297:Male; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index
chemical_list: C491541:Ccl25 protein, mouse; D019742:Chemokines, CC; D012333:RNA, Messenger