Complement in local biliary tract defense: Dissociation between bile complement and acute phase reactants in cholecystitis

Wilton, Peter B.; Dalmasso, Agustin P.; Allen, Melody O'Connor

doi:10.1016/0022-4804(87)90179-x

Cited by 10 publications

(6 citation statements)

References 13 publications

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“…Aliquots of fibronectin diluted in prefiltered PBS (0.2-μπι sterile Minisart filters) were added in duplicate to 500-μΐ prefiltered (0.2-μηι filters) model bile in 1.5-ml screw cup sterile Eppendorf tubes to yield final concentrations of 0.5, 1.2, 10, 20, and 40 μg/ml (n = 4 for each concentration). These concentrations cover the range of fibronectin concentrations found by us and others (7,41) in gallbladder bile. Equal aliquots of PBS but without fibronectin were added to model bile as controls.…”

Section: Chemicals and Reagentssupporting

confidence: 77%

“…The concentrations of fibronectin in human gallblad der bile from cholesterol gallstone patients measured with an immunofluorometric assay (19) were in the same range as the concentrations previously described for gallstone patients using other methods (7,41). In addition, we have found with immunoblot analysis using specific polyclonal and monoclonal antibodies against plasma fibronectin that bile fibronectin was antigenically intact and showed a similar molecular mass to plasma fibronectin (i.e., a doublet with 220 kDa under reducing conditions).…”

Section: Discussionsupporting

confidence: 66%

“…Gallbladder inflammation is a frequent finding in gallstone patients. Biliary fibronectin appears to be higher in acute cholecys titis than in chronic cholecystitis and stone-free patients (7,41). Increased levels of fibronectin have been mea sured in body fluids other than plasma as a consequence of epithelial damage and/or inflammation (19,31,34).…”

Section: Discussionmentioning

confidence: 99%

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Fibronectin in human gallbladder bile: cholesterol pronucleating and/or mucin "link" protein?

Miquel

Ritter

Pozo

et al. 1994

American Journal of Physiology-Gastrointestinal and Liver Physi

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Some biliary proteins (pronucleators) seem to be essential factors for cholesterol crystal formation and crystal growth in bile. A recent study suggests that fibronectin is such a pronucleator in bile. Fibronectin also seems to closely interact with intestinal mucin. Since biliary mucin plays an important role in gallstone formation, such an interaction in bile may be of relevance in cholesterol gallstone formation. To more clearly elucidate the role of fibronectin in cholesterol gallstone disease, we measured the concentration of fibronectin in native bile of cholesterol gallstone patients and checked its influence on the cholesterol nucleation time of model bile. We further looked for a molecular interaction between biliary fibronectin and gallbladder mucin. We found that fibronectin is present in gallbladder bile of gallstone patients in low concentrations (2.6 +/- 1.2 micrograms/ml). Bile fibronectin did not interact with gallbladder mucin. Moreover, in a wide range of concentrations fibronectin had no influence on the nucleation time of model bile. We conclude that fibronectin does not seem to play a major role in cholesterol gallstone disease.

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Section: Chemicals and Reagentssupporting

confidence: 77%

Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

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Fibronectin in human gallbladder bile: cholesterol pronucleating and/or mucin "link" protein?

Miquel

Ritter

Pozo

et al. 1994

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In fact, a growing body of evidence points to the presence of a range of inflammatory mediators and other factors in bile. These factors include epidermal growth factor (21), cytokines TNF-␣ and IL-6 (37,40), and IL-1␣ and IL-1␤ (M. Wiseman, W. Sewell, and G. D. F. Jackson, unpublished data), complement proteins, and acute-phase proteins (46). Although the harsh conditions in which they are found might argue against a functional role for these biliary mediators, recent evidence suggests they may remain active within the lumen of the gastrointestinal tract (13, 36; W. Sewell, Y. Dai, and G. D. F. Jackson, unpublished data).…”

Section: Discussionmentioning

confidence: 99%

“…The liver is the usual site of LPS clearance (10) and is an important site of production of cytokines (25,33,44) and other mediators of inflammation (46). Such mediators have been detected in bile (37,40), and we have previously described a role for the hepatobiliary system in models of gastrointestinal inflammation (3).…”

mentioning

confidence: 99%

Lipopolysaccharide-Induced Biliary Factors Enhance Invasion ofSalmonella enteritidisin a Rat Model

et al. 2000

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In this study, the role of the hepatobiliary system in the early pathogenesis of Salmonella enteritidis infection was investigated in a rat model. Intravenous (i.v.) challenge with lipopolysaccharide (LPS) has previously been shown to enhance the translocation of normal gut flora. We first confirmed that LPS can similarly promote the invasion of S. enteritidis. Oral infection of outbred Australian Albino Wistar rats with 10 6 to 10 7 CFU of S. enteritidis led to widespread tissue invasion after days. If animals were similarly challenged after intravenous administration of S. enteritidis LPS (3 to 900 g/kg of body weight), significant invasion of the livers and mesenteric lymph nodes (MLN) occurred within 24 h, with invasion of the liver increasing in a dose-dependent fashion (P < 0.01). If bile was prevented from reaching the intestine by bile duct ligation or cannulation, bacterial invasion of the liver and MLN was almost totally abrogated (P < 0.001). As i.v. challenge with LPS could induce the delivery of inflammatory mediators into the bile, biliary tumor necrosis factor alpha (TNF-␣) concentrations were measured by bioassay. Biliary concentrations of TNF-␣ rose shortly after LPS challenge, peaked with a mean concentration of 27.0 ng/ml at around 1 h postchallenge, and returned to baseline levels (3.1 ng/ml) after 2.5 h. Although TNF-␣ cannot be directly implicated in the invasion process, we conclude that the invasiveness of the enteric pathogen S. enteritidis is enhanced by the presence of LPS in the blood and that this enhanced invasion is at least in part a consequence of the delivery of inflammatory mediators to the gastrointestinal tract by the hepatobiliary system.

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Characterization of complement C3, C4, and factor B molecules in human bile

et al. 1997

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We performed molecular analysis of complement components (C3, C4, and factor B) in human bile by sodium dodecyl sulfate-polyarylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Complement C3 was detected as a molecule composed of a 115-kDa alpha-chain linked to a 70-kDa beta-chain by disulfide bonds, and C3 levels ranged from 45 to 650 micrograms/ml (n = 15). C4 was detected as a triple chain (98-kDa alpha-chain, 73-kDa beta-chain, and 33-kDa gamma-chain) molecule linked by disulfide bonds, and C4 levels ranged from 2.5 to 60 micrograms/ml. Factor B, a component of the alternative pathway, was also detected, as an intact form. Factor B levels ranged from 0.3 to 8.0 micrograms/ml. The sizes and subunit structures of complement components in human bile were compatible with those reported in human serum. The results of a hemolytic assay indicated that complement molecules in human bile were functionally active. These molecules may participate in local immune and inflammatory responses in the biliary tract.

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Complement in local biliary tract defense: Dissociation between bile complement and acute phase reactants in cholecystitis

Cited by 10 publications

References 13 publications

Fibronectin in human gallbladder bile: cholesterol pronucleating and/or mucin "link" protein?

Fibronectin in human gallbladder bile: cholesterol pronucleating and/or mucin "link" protein?

Lipopolysaccharide-Induced Biliary Factors Enhance Invasion ofSalmonella enteritidisin a Rat Model

Characterization of complement C3, C4, and factor B molecules in human bile

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