Tags

Type your tag names separated by a space and hit enter

Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome.
Pediatr Surg Int. 2002 Oct; 18(7):615-9.PS

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.

Authors+Show Affiliations

Sukhotnik I
Rappoport Faculty of Medicine, Technion, Israel. igor-dr@internet-zahav.net
Yakirevich E
No affiliation info available
Coran AG
No affiliation info available
Siplovich L
No affiliation info available
Krausz M
No affiliation info available
Sabo E
No affiliation info available
Kramer A
No affiliation info available
Shiloni E
No affiliation info available

MeSH

Adaptation, PhysiologicalAnimalsApoptosisCell DivisionEndotoxemiaEnterocytesLipopolysaccharidesMaleRatsRats, Sprague-DawleyShort Bowel Syndrome

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12471477

Citation

Sukhotnik, I, et al. "Lipopolysaccharide Endotoxemia Reduces Cell Proliferation and Decreases Enterocyte Apopotosis During Intestinal Adaptation in a Rat Model of Short-bowel Syndrome." Pediatric Surgery International, vol. 18, no. 7, 2002, pp. 615-9.
Sukhotnik I, Yakirevich E, Coran AG, et al. Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome. Pediatr Surg Int. 2002;18(7):615-9.
Sukhotnik, I., Yakirevich, E., Coran, A. G., 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), 615-9.
Sukhotnik I, et al. Lipopolysaccharide Endotoxemia Reduces Cell Proliferation and Decreases Enterocyte Apopotosis During Intestinal Adaptation in a Rat Model of Short-bowel Syndrome. Pediatr Surg Int. 2002;18(7):615-9. PubMed PMID: 12471477.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lipopolysaccharide endotoxemia reduces cell proliferation and decreases enterocyte apopotosis during intestinal adaptation in a rat model of short-bowel syndrome. AU - Sukhotnik,I, AU - Yakirevich,E, AU - Coran,A G, AU - Siplovich,L, AU - Krausz,M, AU - Sabo,E, AU - Kramer,A, AU - Shiloni,E, Y1 - 2002/09/26/ PY - 2001/11/28/accepted PY - 2002/12/10/pubmed PY - 2003/5/7/medline PY - 2002/12/10/entrez SP - 615 EP - 9 JF - Pediatric surgery international JO - Pediatr Surg Int VL - 18 IS - 7 N2 - 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. SN - 0179-0358 UR - https://www.unboundmedicine.com/medline/citation/12471477/Lipopolysaccharide_endotoxemia_reduces_cell_proliferation_and_decreases_enterocyte_apopotosis_during_intestinal_adaptation_in_a_rat_model_of_short_bowel_syndrome_ DB - PRIME DP - Unbound Medicine ER -