Differential effects of chenodeoxycholic and ursodeoxycholic acids on expression of procoagulant activity by human monocytes

Calmus, Yvon; Podevin, Philippe; Robert, Annie; Poupon, Raoul

doi:10.1016/s0168-8278(05)80491-x

Cited by 13 publications

(11 citation statements)

References 35 publications

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“…UDCA inhibits cytokine production by human monocytes (68). However, according to another study, chenodeoxycholic acid inhibited cytokine production from monocytes even more actively and UDCA in part decreased the effect of chenodeoxycycholic acid (69,70). At present, the (67).…”

Section: Mechanism Of Action Of Udcamentioning

confidence: 89%

“…Furthermore, UDCA inhibits the absorption of endogenous bile acids in the intestine (60) and changes the balance between hydrophobic, toxic bile acids and hydrophilic, untoxic bile acids in favour of hydrophilic bile acids (61-66). This may be a key mechanism responsible for the beneficial effect of UDCA A variety of effects of UDCA on the immune system were observed, which in part indicate immunosuppression (68) and in part a decrease of immunosuppressive effects induced by other bile acids (69,70). In PBC (71) and PSC (72), an increased expression of HLA antigens on hepatocytes may be related to the hepatic damage in these diseases because it represents a prerequisite for the action of cytotoxic T-lymphocytes.…”

Section: Mechanism Of Action Of Udcamentioning

confidence: 99%

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Ursodeoxycholic Acid in the Treatment of Primary Sclerosing Cholangitis

Stiehl

1994

Annals of Medicine

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Primary sclerosing cholangitis (PSC) is a cholestatic liver disease characterized by inflammation and obliterative fibrosis of bile ducts leading to their progressive destruction (1-4). As a consequence, cholestasis with elevated serum levels of alkaline phosphatase (AP) and gamme glutamyl transpeptidase (GGT) and bilirubin in more advanced disease is the most prominent feature of this disease. The diagnosis of PSC is primarily based on endoscopic retrograde cholangiography with demonstration of irregular strictures and dilatations. In liver biopsy, typical findings are portal and periodical inflammation and fibrosis. Since PSC is a focal disease, the characteristic histological findings may or may not be seen in a single liver biopsy. The cause of PSC is still unknown. The association with histocombatibility antigens indicates that immunological mechanisms may be involved but it is still unclear whether the disease is immunogenic. Alternatively, bacteria and bacterial toxins from the colon might play a role (3, 4). In 70% of cases PSC is associated with ulcerative colitis (5) and, therefore, in all patients with this intestinal disease who also have elevated levels of liver enzymes, a cholangiography should be performed. Recently, in up to 80% of patients with PSC anti-neutrophil-cytoplasmatic-antigens (ANCA) were found to be elevated (6) and, in future, this test may help to diagnose the disease more easily. Up to now, however, the disease is usually diagnosed at a relatively advanced stage when the patients have jaundice.

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Section: Mechanism Of Action Of Udcamentioning

confidence: 89%

Section: Mechanism Of Action Of Udcamentioning

confidence: 99%

Ursodeoxycholic Acid in the Treatment of Primary Sclerosing Cholangitis

Stiehl

1994

Annals of Medicine

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“…For example, CDCA at 100 to 250 mol/L inhibited procoagulant activity and production of IL-6 or TNF-␣ from human monocytes, whereas UDCA did not. 19,43 TC-DCA at 500 mol/L inhibited N-formyl-methionyl-leucylphenylalanine-induced cytosolic Ca 2ϩ levels in neutrophils, whereas TUDCA did not. 22 Interestingly, UDCA suppresses immunoglobulin production and the produc- tion of IL-2, IL-4, and interferon-␥ from lymphocytes.…”

Section: Figmentioning

confidence: 94%

Bile acids induce eosinophil degranulation by two different mechanisms

Yamazaki¹

2001

Hepatology

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Eosinophil infiltration and activation occur in the vicinity of the bile ducts in immune cholangiopathies. When cholangiocytes are injured, bile acids may cross the damaged biliary epithelia and affect periductal immune cells. Although immunomodulatory actions of bile acids have been well explored, their effects on eosinophils have never been examined. In this study, we tested the hypothesis that bile acids directly activate eosinophils and induce their effector functions. We found that a hydrophobic bile acid, taurine-conjugated chenodeoxycholic acid (TCDCA), induces eosinophil degranulation in vitro via 2 different mechanisms depending on its concentration. Degranulation induced by 100 to 500 mol/L TCDCA was an active and regulated release because it was completely abolished by a tyrosine kinase inhibitor (genistein), by a microfilament inhibitor (cytochalasin B), and by incubation at 4°C. Furthermore, eosinophils stimulated with 10 to 250 mol/L TCDCA vigorously produced superoxide and interleukin-8 (IL-8). In contrast, at higher concentrations (e.g., > 1,000 mol/L), TCDCA induced granule protein release without concomitant superoxide production and IL-8 production. Further genistein and cytochalasin B failed to inhibit eosinophil degranulation induced by 2,500 mol/L TCDCA, suggesting that TCDCA at this concentration induced passive degranulation via cytolysis. The analyses of cell morphology and functional viability also supported the presence of 2 mechanisms for TCDCA-induced eosinophil degranulation. Taurine-conjugated ursodeoxycholic acid, a hydrophilic bile acid, similarly activated human eosinophils at relatively low concentrations, although the potency was always lower compared with that of TCDCA. In conclusion, we have shown that bile acids are capable of directly activating eosinophils. (HEPATOLOGY 2001;33:582-590.)

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“…Whereas Yoshikawa et al 24 reported that UDCA suppresses immunoglobulin and IL-2 and IL-4 production by stimulated peripheral blood mononuclear cells, others have found no effect of UDCA on immune function. 25,26 Others have found that UDCA attenuates the production of nitric oxide by inhibiting production of nitric oxide synthase. 27 It has been suggested that PBC may be triggered by a transmissable agent, possibly a virus 28 ; that nitric oxide is a potent inhibitor of cytokine production (including RANTES, granulocytemacrophage colony-stimulating factor, and IL-8) and of viral replication 29 may suggest why UDCA could have a therapeutic role even in a disease triggered by a virus.…”

mentioning

confidence: 99%

“…For example, on mast cells: ursodeoxycholylglycine activates mast cells to a lesser extent than chenodeoxycholylglycine or deoxycholylglycine. 30 On monocytes, Lacaille and Paradis 31 and Calmus et al 25,26 found that bile acids inhibit monocyte activation and T lymphocyte proliferative responses, but this inhibition was reversed by UDCA. UDCA normalizes the defective natural killer activity, reduced by the hydrophobic bile acids, by inhibiting prostaglandin E2 production.…”

mentioning

confidence: 99%

Eosinophils and primary biliary cirrhosis?Stoking the fire?

Neuberger

1999

Hepatology

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Differential effects of chenodeoxycholic and ursodeoxycholic acids on expression of procoagulant activity by human monocytes

Cited by 13 publications

References 35 publications

Ursodeoxycholic Acid in the Treatment of Primary Sclerosing Cholangitis

Ursodeoxycholic Acid in the Treatment of Primary Sclerosing Cholangitis

Bile acids induce eosinophil degranulation by two different mechanisms

Eosinophils and primary biliary cirrhosis?Stoking the fire?

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