Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome
dc.contributor.author | Sukhotnik, Igor | en_US |
dc.contributor.author | Yakirevich, E. | en_US |
dc.contributor.author | Shiloni, Eitan | en_US |
dc.contributor.author | Krausz, M. | en_US |
dc.contributor.author | Kramer, Alexander | en_US |
dc.contributor.author | Siplovich, L. | en_US |
dc.contributor.author | Coran, Arnold G. | en_US |
dc.contributor.author | Sabo, E. | en_US |
dc.date.accessioned | 2006-09-08T20:04:33Z | |
dc.date.available | 2006-09-08T20:04:33Z | |
dc.date.issued | 2002-10 | en_US |
dc.identifier.citation | Sukhotnik, I.; Yakirevich, E.; Coran, A.; Siplovich, L.; Krausz, M.; Sabo, E.; Kramer, A.; Shiloni, E.; (2002). "Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome." Pediatric Surgery International 18(7): 615-619. <http://hdl.handle.net/2027.42/42198> | en_US |
dc.identifier.issn | 0179-0358 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/42198 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12471477&dopt=citation | en_US |
dc.description.abstract | Sepsis is frequently associated with or complicates short-bowel syndrome (SBS). To investigate the effects of lipopolysaccharide (LPS) endotoxemia on enterocyte proliferation and death via apoptosis in a rat model of SBS, adult male Sprague-Dawley rats were divided into three experimental groups: sham rats underwent bowel transection and reanastomosis; SBS rats underwent 75% small-bowel resection; and SBS-LPS rats underwent 75% bowel resection and were given intraperitoneal injections of LPS 10 mg/kg. Parameters of intestinal adaptation (bowel and mucosal weights, mucosal DNA and protein, villus height, and crypt depth), enterocyte proliferation, and death via apoptosis were determined on day 15 after the operation. Statistical analysis was determined by Student's and ANOVA tests with a P less than 0.05 considered significant. SBS-LPS animals demonstrated a significant decrease (vs SBS rats) in duodenal (20%), jejunal (30%), and ileal (15%) overall weight, duodenal (20%), jejunal (27%), and ileal (18%) mucosal weight, jejunal (20%) and ileal (30%) mucosal DNA, jejunal (29%) and ileal (31%) villus height, and jejunal (14%) and ileal (29%) crypt depth. LPS endotoxemia led to reduced cell proliferation and enterocyte apoptosis compared to untreated SBS animals. Thus, in a rat model of SBS, LPS endotoxemia inhibits intestinal adaptation. A possible mechanism may be decreased cell proliferation. Decreased enterocyte loss via apoptosis may reflect a reduced number of enterocytes. Other mechanisms (necrosis) may be mainly responsible for cell death following LPS injection. | en_US |
dc.format.extent | 424781 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag | en_US |
dc.subject.other | Short-bowel Syndrome Intestinal Adaptation Lipopolysaccharide Endotoxemia | en_US |
dc.subject.other | Legacy | en_US |
dc.title | Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Pediatrics | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Section of Pediatric Surgery, C.S. Mott Children's Hospital and University of Michigan Medical School, Ann Arbor, MI, USA, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationother | Rappaport Faculty of Medicine, Technion, Carmel Medical Center, HaEmek, Medical Center and Rambam Medical Center, Haifa, Israel, | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 12471477 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/42198/1/s00383-002-0862-8.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/s00383-002-0862-8 | en_US |
dc.identifier.source | Pediatric Surgery International | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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