title: Pseudomonas pneumonia-mediated sepsis induces expression of pancreatitis-associated protein-I in rat pancreas.
abstract: Severe impairment of exocrine pancreatic secretion has recently been demonstrated in a clinical study in sepsis and septic shock patients. The purpose of this study was to further evaluate involvement of the pancreas in the acute phase reaction in sepsis. Using a normotensive rat model of Pseudomonas pneumonia-induced sepsis, we assessed the expression of PAP-I, amylase and trypsinogen mRNA, PAPI protein levels, and cytokine expression in the pancreas by Northern and Western blot analysis and RT-M PCR, respectively. Presence of several well-established features of pancreatitis in sepsis-induced animals were examined by biochemical and histopathological methods as well as by a determination of both water and myeloperoxidase content. Sepsis resulted in an up-regulation of PAP-I gene expression and increase in its protein level in pancreas while the mRNA levels of amylase and trypsinogen were down-regulated. Differences in the pancreatic cytokine expression, serum amylase and serum lipase levels, the occurrence of pancreatic edema as well as the severity of inflammatory infiltration and necrosis were not significantly different between sham and pneumonia groups. Acinar cells showed increased vacuolization in pneumonia animals 24 hours after the treatment. These findings demonstrate that the pancreas is actively involved in the acute phase reaction in sepsis of remote origin. This involvement occurs without concomitant biochemical and histopathologic alterations observed in pancreatitis. Taken all together, these features are indicative of a sepsis-specific dysfunction of the pancreas.
authors.affiliation: Sunnybrook and Women's College Health Sciences Centre and University of Toronto, Toronto, Ontario, Canada. barbara.tribl@gmx.at
authors.forename: Barbara
authors.initials: B
authors.lastname: Tribl
authors.forename: Dominik
authors.initials: D
authors.lastname: Filipp
authors.forename: Hans
authors.initials: H
authors.lastname: Bödeker
authors.forename: Pei
authors.initials: P
authors.lastname: Yu
authors.forename: Irene
authors.initials: I
authors.lastname: Hammerrmüller
authors.forename: Colin
authors.initials: C
authors.lastname: McKerlie
authors.forename: Volker
authors.initials: V
authors.lastname: Keim
authors.forename: William J
authors.initials: WJ
authors.lastname: Sibbald
mesh_terms: D000210:Acute-Phase Reaction / Q000235:genetics; D000681:Amylases / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D000818:Animals; D000951:Antigens, Neoplasm / Q000096:biosynthesis* / Q000235:genetics; D014408:Biomarkers, Tumor / Q000096:biosynthesis* / Q000235:genetics; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D005786:Gene Expression Regulation; D037181:Lectins, C-Type / Q000096:biosynthesis* / Q000235:genetics; D007958:Leukocyte Count; D008049:Lipase / Q000097:blood; D008297:Male; D009336:Necrosis; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D010195:Pancreatitis / Q000209:etiology*; D000073718:Pancreatitis-Associated Proteins; D009195:Peroxidase / Q000032:analysis; D018410:Pneumonia, Bacterial / Q000150:complications*; D011552:Pseudomonas Infections / Q000150:complications / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000209:etiology / Q000378:metabolism*; D013997:Time Factors; D014362:Trypsinogen / Q000096:biosynthesis / Q000235:genetics; D014617:Vacuoles / Q000648:ultrastructure
chemical_list: D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; D016207:Cytokines; D037181:Lectins, C-Type; D000073718:Pancreatitis-Associated Proteins; C000612141:REG3A protein, human; D012333:RNA, Messenger; C000612144:Reg3b protein, rat; D014362:Trypsinogen; D009195:Peroxidase; D008049:Lipase; D000681:Amylases