Endotoxemia in human obstructive jaundice

Ingoldby, C. J. H.; McPherson, G. A. D.; Blumgart, L.H.

doi:10.1016/0002-9610(84)90197-1

Cited by 52 publications

(22 citation statements)

References 12 publications

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“…Our results agree with those of past studies where no variation in endotoxin levels was noted [4,8]. It has been proved that after the settlement of jaundice followed by endotoxinemia, the bilirubin and aminotransferase levels were significantly decreased (Tables 5 and 7) [10,11].…”

Section: Discussionsupporting

confidence: 92%

“…However, other authors [4,5,8,9] suggest alternative mechanisms in the pathogenesis of endotoxinemia in obstructive jaundice. Levels of endotoxin rising from 15% to 70% are associated with the disease [4,5,8,9].…”

Section: Discussionmentioning

confidence: 98%

“…Previous clinical studies [3][4][5]8] suggest that flow of the gastrointestinal bile salt enhances portal absorption of intestinally derived endotoxin.…”

Section: Discussionmentioning

confidence: 99%

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Endotoxinemia in the portal and the systemic circulation in obstructive jaundice

Papakostas

Bezirtzoglou

Pitiakoudis

et al. 2003

Clinical and Experimental Medicine

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Endotoxinemia in patients with obstructive jaundice is linked to acute renal failure and sepsis and remains a major cause of complications during postoperative treatment. The current study examines the mechanisms of endotoxinemia in the portal and the systemic circulation in obstructive jaundice. As an experimental model of the disease we used rabbits subjected to sham operation. Serum total bilirubin aminotransferases and endotoxin concentrations were determined at 2, 5, 8, and 13 days after operation. Endotoxin concentrations were estimated by the limulus lysate endotoxin test. A high frequency of portal or systemic endotoxinemia is observed in obstructive jaundice, but no difference between endotoxinemia levels in the portal and systemic circulation was observed.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 98%

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Endotoxinemia in the portal and the systemic circulation in obstructive jaundice

Papakostas

Bezirtzoglou

Pitiakoudis

et al. 2003

Clinical and Experimental Medicine

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“…It has been demonstrated that endotoxemia often occurs together with cholestasis (5,8), suggesting a potential relationship between bile salt and endotoxemia in cholestasis. Indeed, it has been reported that obstructive jaundice can increase bacterial translocation (9).…”

mentioning

confidence: 99%

LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in mice

Isayama¹,

Hines²,

Kremer³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

117

102

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Although it is clear that bile acid accumulation is the major initiator of fibrosis caused by cholestatic liver disease, endotoxemia is a common side effect. However, the depletion of hepatic macrophages with gadolinium chloride blunts hepatic fibrosis. Because endotoxin is a key activator of hepatic macrophages, this study was designed to test the hypothesis that LPS signaling through CD14 contributes to hepatic fibrosis caused by experimental cholestasis. Wild-type mice and CD14 knockout mice (CD14(-/-)) underwent sham operation or bile duct ligation and were killed 3 wk later. Measures of liver injury, such as focal necrosis, biliary cell proliferation, and inflammatory cell influx, were not significantly different among the strains 3 wk after bile duct ligation. Markers of liver fibrosis such as Sirius red staining, liver hydroxyproline, and alpha-smooth muscle actin expression were blunted in CD14(-/-) mice compared with wild-type mice after bile duct ligation. Despite no difference in lymphocyte infiltration, the macrophage/monocyte activation marker OX42 (CD11b) and the oxidative stress/lipid peroxidation marker 4-hydroxynonenal were significantly upregulated in wild-type mice after bile duct ligation but not in CD14(-/-) mice. Increased profibrogenic cytokine mRNA expression in the liver after bile duct ligation was significantly blunted in CD14(-/-) mice compared with the wild type. The hypothesis that LPS was involved in experimental cholestatic liver fibrosis was tested using mice deficient in LPS-binding protein (LBP(-/-)). LBP(-/-) mice had less liver injury and fibrosis (Siruis red staining and hydroxyproline content) compared with wild-type mice after bile duct ligation. In conclusion, these data demonstrate that endotoxin in a CD14-dependent manner exacerbates hepatic fibrogenesis and macrophage activation to produce oxidants and cytokines after bile duct ligation.

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“…95,96 Elevated levels of circulating endotoxin have been found by a number of investigators. [97][98][99][100] Therefore, the prevention of postoperative endotoxemia may reduce the incidence of complications after surgery in these patients.…”

Section: Future Strategiesmentioning

confidence: 99%

Potential applications of N-terminal recombinant fragments of bactericidal/permeability-increasing protein in liver surgery

et al. 1999

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Bactericidal/permeability-increasing protein (BPI) was first isolated by Elsbach and Weiss in 1978. 1,2 It is a natural host-defense protein of 55 kd found in the azurophilic granules of human neutrophils, which are important in the host defense against infections. The protein was named after one of its first discovered properties, the potential to kill bacteria by increasing the permeability of their cell walls. 1,2 This ability to kill bacteria has led to further studies of the functions of BPI, from which researchers have discovered several potentially useful properties. In this article, we first give a brief review of the most important in vitro and in vivo studies showing the functions and properties of BPI and then focus on the potential applications of one of the more stable recombinant BPIs, rBPI 21 , in the field of liver surgery and transplantation. The Main Effects of BPI Antibacterial ActionBPI shows antimicrobial activity against a wide range of gram-negative bacteria. 1-3 The cell envelope of gram-negative bacteria consists of the cytoplasmic membrane, peptidoglycan layer, and an additional barrier, the outer membrane, which is strictly asymmetric with respect to its lipid composition. The outer leaflet of this membrane is composed mainly of lipopolysaccharides (LPS; endotoxins). LPS consists of an oligosaccharide or polysaccharide and a covalently linked glycolipid component (lipid A) that anchors the LPS in the outer membrane. 4 The selectivity of BPI against gram-negative bacteria has been attributed to the strong attraction of BPI for this LPS in the bacterial envelope, especially the high affinity for its lipid A component. 5,6 It has become evident that the LPS structure primarily determines bacterial sensitivity. Strains bearing LPS with short polysaccharide chains in their outer membrane are the most sensitive. Long polysaccharide chains sterically hinder the access of BPI to the binding sites in the inner core and the lipid A regions of LPS, thereby reducing the affinity of BPI for the envelope LPS, necessitating higher ambient BPI concentrations to achieve the required amount of bound BPI to produce its biological effects. 3,6,7 The cytotoxic effect of BPI on gram-negative bacteria can be divided into two stages. When BPI binds to the outer membrane, several immediate effects are manifest, including arrest of bacterial growth, discrete changes in the permeability of the outer membrane, and selective activation of several envelope enzymes, which degrade phospholipids and peptidoglycans. These changes are evident despite preservation of the functional integrity of the biochemical machinery in the nongrowing bacteria. In fact, certain manipulations result in repair of the envelope alterations and resumption of growth, therefore indicating that the initial effects of BPI are not directly bactericidal. 2,8 However, when this process is continued, alterations of the cytoplasmic membrane are produced, resulting in an impairment of the energy metabolism that leads to an irreversible growth arre...

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Endotoxemia in human obstructive jaundice

Cited by 52 publications

References 12 publications

Endotoxinemia in the portal and the systemic circulation in obstructive jaundice

Endotoxinemia in the portal and the systemic circulation in obstructive jaundice

LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in mice

Potential applications of N-terminal recombinant fragments of bactericidal/permeability-increasing protein in liver surgery

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