Ascending cholangitis provokes IL-8 and MCP-1 expression and promotes inflammatory cell infiltration in the cholestatic rat liver

Hsieh, Chih Sung; Huang, Chao; Wu, Jiunn Jong; Chaung, Hso Chi; Wu, Chia Ling; Chang, Nyuk Kong; Chang, Yen Mei; Chou, Ming Huei; Chuang, Jiin Haur

doi:10.1053/jpsu.2001.27933

Cited by 23 publications

(17 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hsieh and colleagues have previously shown increased MCP-1 expression in BDL rats treated with Roux-en-Y choledochojejunostomy and E. coli-induced cholangitis. 33 In our experiments, as well as MCP-1 protein expression, elevated MCP-1 mRNA expression was seen prior to histological hepatic fibrosis (six-fold increase on day 3, peaking at 15.8-fold at 2 weeks, and returning to control levels after 18 weeks), biliary MCP-1 levels were increased versus controls, and serum and biliary MCP-1 levels and biliary TCA concentration all negatively correlated with fibrosis. Of note, MCP-1 mRNA expression preceded the expression of both ␣-SMA (7 days) and procollagen ␣ 1 (I) (2 weeks) mRNA, which are established markers of HSC activation.…”

Section: Discussionsupporting

confidence: 60%

Fibrogenesis in pediatric cholestatic liver disease: Role of taurocholate and hepatocyte-derived monocyte chemotaxis protein-1 in hepatic stellate cell recruitment #

et al. 2009

View full text Add to dashboard Cite

Cholestatic liver diseases, such as cystic fibrosis (CF) liver disease and biliary atresia, predominate as causes of childhood cirrhosis. Despite diverse etiologies, the stereotypic final pathway involves fibrogenesis where hepatic stellate cells (HSCs) are recruited, producing excess collagen which initiates biliary fibrosis. A possible molecular determinant of this recruitment, monocyte chemotaxis protein-1 (MCP-1), an HSC-responsive chemokine, was investigated in CF liver disease and biliary atresia. The bile-duct-ligated rat and in vitro coculture models of cholestatic liver injury were used to further explore the role of MCP-1 in HSC recruitment and proposed mechanism of induction via bile acids. In both CF liver disease and biliary atresia, elevated hepatic MCP-1 expression predominated in scar margin hepatocytes, closely associated with activated HSCs, and was also expressed in cholangiocytes. Serum MCP-1 was elevated during early fibrogenesis. Similar observations were made in bile-duct-ligated rat liver and serum. Hepatocytes isolated from cholestatic rats secreted increased MCP-1 which avidly recruited HSCs in coculture. This HSC chemotaxis was markedly inhibited in interventional studies using anti-MCP-1 neutralizing antibody. In CF liver disease, biliary MCP-1 was increased, positively correlating with levels of the hydrophobic bile acid, taurocholate. In cholestatic rats, increased MCP-1 positively correlated with taurocholate in serum and liver, and negatively correlated in bile. In normal human and rat hepatocytes, taurocholate induced MCP-1 expression. Conclusion: These observations support the hypothesis that up-regulation of hepatocyte-derived MCP-1, induced by bile acids, results in HSC recruitment in diverse causes of cholestatic liver injury, and is a key early event in liver fibrogenesis in these conditions. Therapies aimed at neutralizing MCP-1 or bile acids may help reduce fibro-obliterative liver injury in childhood cholestatic diseases.

show abstract

Section: Discussionsupporting

confidence: 60%

Fibrogenesis in pediatric cholestatic liver disease: Role of taurocholate and hepatocyte-derived monocyte chemotaxis protein-1 in hepatic stellate cell recruitment #

et al. 2009

View full text Add to dashboard Cite

show abstract

“…However, few easily approachable biliary routes have been presented. We have also performed the modifi ed procedure of Rudnicki et al [16] , with a subcutaneous distal jejunostomy tube inserted into the bilioenteric anastomosis [12] . E. coli were injected into this bilioenteric duct via the jejunostomy tube to induce ascending cholangitis after biliary drainage.…”

Section: Discussionmentioning

confidence: 99%

“…The reversibility of cholestasis by biliodigestive anastomosis is technically diffi cult in the rat, with associated high mortality rates [9][10][11] . Ascending cholangitis in the cholestatic rat, with the administration of Escherichia coli via a subcutaneously placed enterostomy catheter into the bilioenteric duct following bilioenteric anastomosis for bile duct obstruction, has been designed for short-term studies [12] .…”

Section: Introductionmentioning

confidence: 99%

Reversible Cholestasis and Cholangitis Induced by Biliary Drainage and Infusion in the Rat

Hsien

Huang²,

Huang³

et al. 2006

Eur Surg Res

View full text Add to dashboard Cite

To develop a rat model of ascending cholangitis, we constructed a controllable and accessible biliary drainage and infusion system. We first modified a reversible cholestasis model of the rat and then induced ascending cholangitis by administration of Escherichia coli into the proximal choledochostomy tube. After biliary infusion of E. coli, the liver, choledochostomy tube and bile were all positive for E. coli, but no bacteria grew in rats receiving biliary infusion of normal saline. Retrograde cholangiography of the initial choledochostomy ensured that the tube end was in the right position in the proximal common bile duct. The patency of the tube-tube choledochocholedochostomy was confirmed by a cholangiogram on day 90. Thirty days after the tube-tube choledochocholedochostomy, the livers of the experimental animals did not differ from the control livers. The tube-tube choledochocholedochostomy model not only provides reproducible, reliable, reversible cholestasis, but creates a sustainable and accessible biliary infusion system. This can be used for long-term investigations of repeated cholangitis and recurrent cholestasis.

show abstract

“…Indeed, DR has been tagged ‘the pace-maker of portal fibrosis’ since proliferating BEC are a source of molecules that activate extracellular matrix (ECM) deposition and secrete pro-inflammatory and chemotactic cytokines, which attract and activate hepatic stellate cells (HSC) and portal fibroblasts 12–14. These and other, yet to be discovered mediators trigger a fibrogenic response and contribute to the progression of liver fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Osteopontin induces ductular reaction contributing to liver fibrosis

Wang

Lopategi

et al. 2014

Gut

106

View full text Add to dashboard Cite

show abstract

Ascending cholangitis provokes IL-8 and MCP-1 expression and promotes inflammatory cell infiltration in the cholestatic rat liver

Cited by 23 publications

References 26 publications

Fibrogenesis in pediatric cholestatic liver disease: Role of taurocholate and hepatocyte-derived monocyte chemotaxis protein-1 in hepatic stellate cell recruitment #

Fibrogenesis in pediatric cholestatic liver disease: Role of taurocholate and hepatocyte-derived monocyte chemotaxis protein-1 in hepatic stellate cell recruitment #

Reversible Cholestasis and Cholangitis Induced by Biliary Drainage and Infusion in the Rat

Osteopontin induces ductular reaction contributing to liver fibrosis

Contact Info

Product

Resources

About