title: Gut-brain chemokine changes in portal hypertensive rats.
abstract: BACKGROUND
  Hepatic encephalopathy is a syndrome whose physiopathology is poorly understood; therefore, current diagnostic tests are imperfect and modern therapy is nonspecific. Particularly, it has been suggested that inflammation plays an important role in the pathogenesis of portal hypertensive encephalopathy in the rat.
  
  
  OBJECTIVE
  We have studied an experimental model of portal hypertension based on a triple partial portal vein ligation in the rat to verify this hypothesis.
  
  
  METHODS
  One month after portal hypertension we assayed in the splanchnic area (liver, small bowel and mesenteric lymph nodes) and in the central nervous system (hippocampus and cerebellum) fractalkine (CX3CL1) and stromal cell-derived factor alpha (SDF1-α) as well as their respective receptors (CX3CR1 and CXCR4) because of their key role in inflammatory processes.
  
  
  RESULTS
  The significant increase of fractalkine in mesenteric lymph nodes (P<0.05) and its receptor (CX3CR1) in the small bowel (P<0.05) and hippocampus (P<0.01), associated with the increased expression of SDF1-α in the hippocampus (P<0.01) and the cerebellum (P<0.01) suggest that prehepatic portal hypertension in the rat induces important alterations in the expression of chemokines in the gut-brain axis.
  
  
  CONCLUSIONS
  The present study revealed that portal hypertension is associated with splanchnic-brain inflammatory alterations mediated by chemokines.
authors.affiliation: Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n, 28040, Madrid, Spain. josem2005@yahoo.es
authors.forename: Joaquin
authors.initials: J
authors.lastname: Merino
authors.forename: Maria-Angeles
authors.initials: MA
authors.lastname: Aller
authors.forename: Sandra
authors.initials: S
authors.lastname: Rubio
authors.forename: Natalia
authors.initials: N
authors.lastname: Arias
authors.forename: Maria-Paz
authors.initials: MP
authors.lastname: Nava
authors.forename: Maria
authors.initials: M
authors.lastname: Loscertales
authors.forename: Jaime
authors.initials: J
authors.lastname: Arias
authors.forename: Jorge-Luis
authors.initials: JL
authors.lastname: Arias
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D000073883:CX3C Chemokine Receptor 1; D002531:Cerebellum / Q000378:metabolism; D054428:Chemokine CX3CL1 / Q000378:metabolism; D054377:Chemokine CXCL12 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D041981:Gastrointestinal Tract / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism; D006975:Hypertension, Portal / Q000378:metabolism*; D020343:Hypertensive Encephalopathy / Q000378:metabolism; D008198:Lymph Nodes / Q000378:metabolism; D008297:Male; D008643:Mesentery / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D019718:Receptors, CXCR4 / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism
chemical_list: D000073883:CX3C Chemokine Receptor 1; C516305:CX3CR1 protein, rat; D054428:Chemokine CX3CL1; D054377:Chemokine CXCL12; D018925:Chemokines; C515256:Cxcl12 protein, mouse; C486264:Cxcr4 protein, rat; D019718:Receptors, CXCR4; D019707:Receptors, Chemokine