title: Intracerebroventricular administration of bacterial lipopolysaccharide prevents the development of acute experimental pancreatitis in the rat.
abstract: BACKGROUND
  Lipopolysaccharides (LPS) are responsible for septic shock but low doses of LPS reduce pancreatic damage produced by caerulein-induced pancreatitis (CIP) in rats. Leptin, produced by adipocytes attenuates the severity of CIP. The aim of this study was to evaluate the effect of intracerebroventricular (i.c.v.) administration of LPS on CIP and plasma leptin level and to investigate the involvement of sensory nerves (SN) in the effects of LPS on CIP.
  
  
  METHODS
  CIP was produced by subcutaneous (s.c.) infusion of caerulein (25 Kg/kg) to conscious rats. SN were deactivated with capsaicin (100 mg/kg s.c.). LPS (0.2, 2, or 20 Kg/rat) were applied to the right cerebral ventricle 30 min prior to CIP.
  
  
  RESULTS
  CIP was manifested by an increase in plasma levels of amylase, lipase, leptin and an anti-inflammatory interleukin 10 (IL-10), (by 400%, 1000%, 700% and 50%, respectively), confirmed by histological examination and accompanied by 40% reduction in pancreatic blood flow. Pretreatment of CIP rats with i.c.v. LPS resulted in significant reduction of CIP accompanied by dose-dependent increase in plasma levels of leptin and IL-10. Deactivation of SN, which by itself failed to affect CIP, completely reversed the beneficial effects of i.c.v. administration of LPS on CIP and reduced plasma leptin and IL-10 concentrations.
  
  
  CONCLUSIONS
  Pretreatment with LPS given i.c.v. prevents the development of caerulein-induced pancreatitis through the activation of SN and though the release of leptin.
authors.affiliation: Physiology, Collegium Medicum, Jagiellonian University Kraków, Poland.
authors.forename: Jolanta
authors.initials: J
authors.lastname: Jaworek
authors.forename: Joanna
authors.initials: J
authors.lastname: Bonior
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Nawrot
authors.forename: Anna
authors.initials: A
authors.lastname: Leja
authors.forename: Ryszard
authors.initials: R
authors.lastname: Sendur
authors.forename: Jerzy
authors.initials: J
authors.lastname: Stachura
authors.forename: Wiesław
authors.initials: W
authors.lastname: Pawlik
authors.forename: Stanisław
authors.initials: S
authors.lastname: Konturek
mesh_terms: D000208:Acute Disease; D017667:Adipocytes / Q000378:metabolism; D000344:Afferent Pathways / Q000187:drug effects / Q000503:physiopathology*; D000681:Amylases / Q000097:blood; D000818:Animals; D002211:Capsaicin / Q000633:toxicity; D002108:Ceruletide / Q000633:toxicity; D004926:Escherichia coli; D007276:Injections, Intraventricular; D016753:Interleukin-10 / Q000097:blood / Q000172:deficiency; D020738:Leptin / Q000097:blood / Q000172:deficiency / Q000502:physiology*; D008049:Lipase / Q000097:blood; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000627:therapeutic use*; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D010195:Pancreatitis / Q000097:blood / Q000139:chemically induced / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D013563:Sympathectomy, Chemical
chemical_list: D020738:Leptin; D008070:Lipopolysaccharides; D016753:Interleukin-10; D002108:Ceruletide; D008049:Lipase; D000681:Amylases; D002211:Capsaicin