Lipopolysaccharide-induced gastrointestinal injury in rats

Role of surface hydrophobicity and bile salts

Elizabeth J. Dial, Jimmy J. Romero, Xavier Villa, David W Mercer, Lenard M. Lichtenberger

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Sepsis of gastrointestinal origin can lead to life-threatening complications in vital organs due to bacterial overgrowth and/or translocation from the lumen into the blood. In a rat model of endotoxemia, changes in surface hydrophobicity (associated with barrier integrity) of the gastrointestinal mucosa were examined. Rats were treated with Escherichia coli lipopolysaccharide (LPS), and gastric and ileal tissue were collected for determination of surface hydrophobicity by contact angle analysis. A role for bile salts in hydrophobicity changes was tested by quantifying bile salts in the lumen of both the stomach and ileum after LPS and by the administration of LPS to bile duct-ligated rats. A single intraperitoneal dose of LPS induced a dose-and time-dependent reduction in hydrophobicity of both the stomach and ileum, with the stomach showing greater sensitivity at an earlier time than the ileum. LPS also induced gastric bleeding, reflux of bile acid into the gastric lumen, and decreased levels of bile salt in the ileum. The LPS-induced reductions in surface hydrophobicity of the stomach were prevented by prior bile duct ligation. We conclude that LPS disrupts gastrointestinal barrier integrity, in part by mechanisms involving bile constituents and an attenuation in the mucosa's hydrophobic characteristics.

Original languageEnglish (US)
Pages (from-to)77-80
Number of pages4
JournalShock
Volume17
Issue number1
DOIs
StatePublished - Jan 1 2002

Fingerprint

Bile Acids and Salts
Hydrophobic and Hydrophilic Interactions
Lipopolysaccharides
Stomach
Ileum
Wounds and Injuries
Bile Ducts
Mucous Membrane
Endotoxemia
Bile
Ligation
Sepsis
Hemorrhage
Escherichia coli

Keywords

  • Contact angle
  • Endotoxin
  • Hemoglobin
  • Ileum
  • Stomach

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Lipopolysaccharide-induced gastrointestinal injury in rats : Role of surface hydrophobicity and bile salts. / Dial, Elizabeth J.; Romero, Jimmy J.; Villa, Xavier; Mercer, David W; Lichtenberger, Lenard M.

In: Shock, Vol. 17, No. 1, 01.01.2002, p. 77-80.

Research output: Contribution to journalArticle

Dial, Elizabeth J. ; Romero, Jimmy J. ; Villa, Xavier ; Mercer, David W ; Lichtenberger, Lenard M. / Lipopolysaccharide-induced gastrointestinal injury in rats : Role of surface hydrophobicity and bile salts. In: Shock. 2002 ; Vol. 17, No. 1. pp. 77-80.
@article{3cd33079b0fc494b81bc78b0275800c2,
title = "Lipopolysaccharide-induced gastrointestinal injury in rats: Role of surface hydrophobicity and bile salts",
abstract = "Sepsis of gastrointestinal origin can lead to life-threatening complications in vital organs due to bacterial overgrowth and/or translocation from the lumen into the blood. In a rat model of endotoxemia, changes in surface hydrophobicity (associated with barrier integrity) of the gastrointestinal mucosa were examined. Rats were treated with Escherichia coli lipopolysaccharide (LPS), and gastric and ileal tissue were collected for determination of surface hydrophobicity by contact angle analysis. A role for bile salts in hydrophobicity changes was tested by quantifying bile salts in the lumen of both the stomach and ileum after LPS and by the administration of LPS to bile duct-ligated rats. A single intraperitoneal dose of LPS induced a dose-and time-dependent reduction in hydrophobicity of both the stomach and ileum, with the stomach showing greater sensitivity at an earlier time than the ileum. LPS also induced gastric bleeding, reflux of bile acid into the gastric lumen, and decreased levels of bile salt in the ileum. The LPS-induced reductions in surface hydrophobicity of the stomach were prevented by prior bile duct ligation. We conclude that LPS disrupts gastrointestinal barrier integrity, in part by mechanisms involving bile constituents and an attenuation in the mucosa's hydrophobic characteristics.",
keywords = "Contact angle, Endotoxin, Hemoglobin, Ileum, Stomach",
author = "Dial, {Elizabeth J.} and Romero, {Jimmy J.} and Xavier Villa and Mercer, {David W} and Lichtenberger, {Lenard M.}",
year = "2002",
month = "1",
day = "1",
doi = "10.1097/00024382-200201000-00013",
language = "English (US)",
volume = "17",
pages = "77--80",
journal = "Shock (Augusta, Ga.)",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Lipopolysaccharide-induced gastrointestinal injury in rats

T2 - Role of surface hydrophobicity and bile salts

AU - Dial, Elizabeth J.

AU - Romero, Jimmy J.

AU - Villa, Xavier

AU - Mercer, David W

AU - Lichtenberger, Lenard M.

PY - 2002/1/1

Y1 - 2002/1/1

N2 - Sepsis of gastrointestinal origin can lead to life-threatening complications in vital organs due to bacterial overgrowth and/or translocation from the lumen into the blood. In a rat model of endotoxemia, changes in surface hydrophobicity (associated with barrier integrity) of the gastrointestinal mucosa were examined. Rats were treated with Escherichia coli lipopolysaccharide (LPS), and gastric and ileal tissue were collected for determination of surface hydrophobicity by contact angle analysis. A role for bile salts in hydrophobicity changes was tested by quantifying bile salts in the lumen of both the stomach and ileum after LPS and by the administration of LPS to bile duct-ligated rats. A single intraperitoneal dose of LPS induced a dose-and time-dependent reduction in hydrophobicity of both the stomach and ileum, with the stomach showing greater sensitivity at an earlier time than the ileum. LPS also induced gastric bleeding, reflux of bile acid into the gastric lumen, and decreased levels of bile salt in the ileum. The LPS-induced reductions in surface hydrophobicity of the stomach were prevented by prior bile duct ligation. We conclude that LPS disrupts gastrointestinal barrier integrity, in part by mechanisms involving bile constituents and an attenuation in the mucosa's hydrophobic characteristics.

AB - Sepsis of gastrointestinal origin can lead to life-threatening complications in vital organs due to bacterial overgrowth and/or translocation from the lumen into the blood. In a rat model of endotoxemia, changes in surface hydrophobicity (associated with barrier integrity) of the gastrointestinal mucosa were examined. Rats were treated with Escherichia coli lipopolysaccharide (LPS), and gastric and ileal tissue were collected for determination of surface hydrophobicity by contact angle analysis. A role for bile salts in hydrophobicity changes was tested by quantifying bile salts in the lumen of both the stomach and ileum after LPS and by the administration of LPS to bile duct-ligated rats. A single intraperitoneal dose of LPS induced a dose-and time-dependent reduction in hydrophobicity of both the stomach and ileum, with the stomach showing greater sensitivity at an earlier time than the ileum. LPS also induced gastric bleeding, reflux of bile acid into the gastric lumen, and decreased levels of bile salt in the ileum. The LPS-induced reductions in surface hydrophobicity of the stomach were prevented by prior bile duct ligation. We conclude that LPS disrupts gastrointestinal barrier integrity, in part by mechanisms involving bile constituents and an attenuation in the mucosa's hydrophobic characteristics.

KW - Contact angle

KW - Endotoxin

KW - Hemoglobin

KW - Ileum

KW - Stomach

UR - http://www.scopus.com/inward/record.url?scp=0036356847&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036356847&partnerID=8YFLogxK

U2 - 10.1097/00024382-200201000-00013

DO - 10.1097/00024382-200201000-00013

M3 - Article

VL - 17

SP - 77

EP - 80

JO - Shock (Augusta, Ga.)

JF - Shock (Augusta, Ga.)

SN - 1073-2322

IS - 1

ER -