LPS-binding protein mediates LPS-induced liver injury and mortality in the setting of biliary obstruction

Minter, Rebecca M.; Bi, Xiaoming; Ben-Josef, Gal; Wang, Tianyi; Hu, Bin; Arbabi, Saman; Hemmila, Mark R.; Wang, Stewart C.; Remick, Daniel G.; Su, Grace L.

doi:10.1152/ajpgi.00041.2008

Cited by 31 publications

(26 citation statements)

References 47 publications

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“…There was no clear difference in the levels between different causes of acute liver failure (whether acetaminophen or non acetaminophen) but the number of patients studied was limited. Our observations are in contrast to other types of chronic liver disease including biliary obstruction and cirrhosis where LBP levels have been reported to be increased (20, 29, 30). …”

Section: Discussioncontrasting

confidence: 99%

Lipopolysaccharide Binding Protein Is Down-Regulated During Acute Liver Failure

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Jinjuvadia

et al. 2012

Dig Dis Sci

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Background and Aims Lipopolysaccharide binding protein is involved in the modulation of acute liver injury and failure from acetaminophen. Although the biological activity of lipopolysaccharide binding protein is concentration dependent, little is known about its levels in acute liver failure. Methods Serum and hepatic lipopolysaccharide binding protein were measured in acute acetaminophen induced liver injury in mice. Serum lipopolysaccharide binding protein was measured in human acute liver failure patients with acetaminophen and non-acetaminophen causes. Results Interestingly, contrary to other diseases, serum and hepatic lipopolysaccharide binding protein levels decreased significantly in mice within 24 hours after acetaminophen induced injury compared to control. (1.6 ± 0.1 vs. 3.5 ± 1.6 ug/ml, acetaminophen vs. control, p < 0.05). Similar decreases were noted in another mouse model of acute liver injury due to carbon tetrachloride. Amongst patients with acute liver failure due to acetaminophen (n=5) and non-acetaminophen (n=5), admission lipopolysaccharide binding protein levels were decreased compared to those of healthy controls (5.4 ± 1.4 vs. 3.2 ± 0.2 ug/ml, normal vs. acute liver failure, p = 0.07) However, the levels were not associated with the etiology of acute liver failure or 3 week outcome. Conclusions Serum and hepatic lipopolysaccharide binding protein levels are significantly reduced early after induction of severe acute liver injury/failure due to acetaminophen and other liver injuries. This reduction in LBP production is specific to acute liver failure and may be important in developing future diagnostic and therapeutic approaches for patients with acute liver failure.

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Section: Discussioncontrasting

confidence: 99%

Lipopolysaccharide Binding Protein Is Down-Regulated During Acute Liver Failure

Fontana

Jinjuvadia

et al. 2012

Dig Dis Sci

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“…Consistent with earlier observations [10,24,25], our current study demonstrates a profound proinflammatory response, characterized by an unregulated production of proinflammatory cytokines and increased neutrophil infiltration, presents in animals with biliary obstruction following sepsis. This proinflammatory milieu is associated with elevated markers of organ injury.…”

Section: Discussionsupporting

confidence: 93%

Human adrenomedullin and its binding protein ameliorate sepsis-induced organ injury and mortality in jaundiced rats

Yang

Zhou

et al. 2010

Peptides

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Sepsis is a serious complication for patients with obstructive jaundice. Although administration of adrenomedullin (AM) in combination with its binding protein (AMBP-1) is protective after injury, it remains unknown whether AM/AMBP-1 ameliorates sepsis-induced organ injury and mortality in the setting of biliary obstruction. The aim of this study is, therefore, to test the efficacy of human AM/AMBP-1 in a rat model of obstructive jaundice and polymicrobial sepsis. To study this, obstructive jaundice was induced in male adult rats (275-325g) by common bile duct ligation (BDL). One week after BDL, the rats were subjected to sepsis by cecal ligation and puncture (CLP). Plasma levels of AM and AMBP-1 were measured at 20 h after CLP. In additional groups of BDL+CLP rats, human AM/AMBP-1 (24/80 µg/kg BW) or vehicle (i.e., human albumin) was administered intravenously at 5 h after CLP. Blood and tissue samples were collected at 20 h after CLP for various measurements. To determine the long-term effect of human AM/AMBP-1 after BDL+CLP, the gangrenous cecum was removed at 20 h after CLP and 7-day survival was recorded. Our results showed that plasma levels of AM were significantly increased while AMBP-1 levels were markedly decreased after BDL+CLP (n=8, P<0.05). Administration of human AM/AMBP-1 attenuated tissue injury and inflammatory responses after BDL+CLP. Moreover, human AM/AMBP-1 significantly increased the survival rate from 21% (n=14) to 53% (n=15). Thus, human AM/AMBP-1 ameliorates sepsis-induced organ injury and mortality in jaundiced rats. Human AM/AMBP-1 can be further developed as a novel treatment for sepsis in jaundiced patients.

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“…The progression of obstructive biliary diseases is associated with proteomic changes, which may be partially due to changes in the blood and tissues composition of patients. For instance, LPS-binding protein mediates LPS-induced liver injury and mortality during biliary obstruction [20]. Proteins are sometimes secreted by cholangiocytes or hepatocytes in response to cholestatic diseases such as BA [21], [22], [23].…”

Section: Discussionmentioning

confidence: 99%

Identification of HSP90 as Potential Biomarker of Biliary Atresia Using Two-Dimensional Electrophoresis and Mass Spectrometry

et al. 2013

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Biliary atresia (BA) is a devastating cholestatic liver disease targeting infants. Current diagnosis depends on surgical exploration of the biliary tree. The aim of the present study was to identify potential biomarkers for the diagnosis of biliary atresia (BA). Two-dimensional electrophoresis was utilized for the identification of proteins that were differentially expressed in liver biopsies of 20 BA patients and 12 infants with non-BA neonatal cholestasis (NC) as controls. Using mass spectrometry, we identified 15 proteins with expressions significantly altered. Out of the 15 proteins identified, heat shock protein (HSP) 90 was the most significantly altered and was down-regulated in BA samples compared to NC samples using immunoblotting analysis. Our findings suggest that HSP90 might be a potential biomarker for the diagnosis of BA and may be used for monitoring further development and therapy for BA. This study demonstrated that a comprehensive strategy of proteomic identification combined with further validation should be adopted in biomarker discovery.

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LPS-binding protein mediates LPS-induced liver injury and mortality in the setting of biliary obstruction

Cited by 31 publications

References 47 publications

Lipopolysaccharide Binding Protein Is Down-Regulated During Acute Liver Failure

Lipopolysaccharide Binding Protein Is Down-Regulated During Acute Liver Failure

Human adrenomedullin and its binding protein ameliorate sepsis-induced organ injury and mortality in jaundiced rats

Identification of HSP90 as Potential Biomarker of Biliary Atresia Using Two-Dimensional Electrophoresis and Mass Spectrometry

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