Soluble intercellular adhesion molecule-1 in primary biliary cirrhosis: effect of ursodeoxycholic acid and immunosuppressive therapy

Ag, Lim; Fh, Wolfhagen; Verma, Ajay; Hr, van Buuren; Rp, Jazrawi; J, Levy; Northfield, T. C.; Sw, Schalm

doi:10.1097/00042737-199702000-00009

Cited by 7 publications

(3 citation statements)

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“…In PBC, ICAM-1 was not only expressed on the basal, but also on the luminal, side of the plasma membrane of bile duct epithelial cells, whereas LFA-1 was detected in lymphocytes around and among damaged bile duct epithelial cells. UDCA therapy reduces ICAM-1 and LFA-1 expression at all of these sites [224], and this effect was additive with that afforded by corticoid therapy [225].…”

Section: Udca-induced Reversal Of Aberrant Expression Of Mhcsmentioning

confidence: 93%

Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications

et al. 2011

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UDCA (ursodeoxycholic acid) is the therapeutic agent most widely used for the treatment of cholestatic hepatopathies. Its use has expanded to other kinds of hepatic diseases, and even to extrahepatic ones. Such versatility is the result of its multiple mechanisms of action. UDCA stabilizes plasma membranes against cytolysis by tensioactive bile acids accumulated in cholestasis. UDCA also halts apoptosis by preventing the formation of mitochondrial pores, membrane recruitment of death receptors and endoplasmic-reticulum stress. In addition, UDCA induces changes in the expression of metabolizing enzymes and transporters that reduce bile acid cytotoxicity and improve renal excretion. Its capability to positively modulate ductular bile flow helps to preserve the integrity of bile ducts. UDCA also prevents the endocytic internalization of canalicular transporters, a common feature in cholestasis. Finally, UDCA has immunomodulatory properties that limit the exacerbated immunological response occurring in autoimmune cholestatic diseases by counteracting the overexpression of MHC antigens and perhaps by limiting the production of cytokines by immunocompetent cells. Owing to this multi-functionality, it is difficult to envisage a substitute for UDCA that combines as many hepatoprotective effects with such efficacy. We predict a long-lasting use of UDCA as the therapeutic agent of choice in cholestasis.

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Section: Udca-induced Reversal Of Aberrant Expression Of Mhcsmentioning

confidence: 93%

Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications

et al. 2011

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“…Accordingly, UDCA increases biliary secretion of bile acids and HCO 3 - and also modulates the expression of BA-detoxification related genes [ 8 , 9 , 10 , 11 ]. Furthermore, UDCA therapy reduces levels of apoptotic cells, inflammatory and fibrotic markers (TNF-α and TGF-β), while inhibiting the overexpression of hepatic MHC-I and adhesion molecules in immune and biliary cells in PBC patients [ 12 , 13 , 14 , 15 , 16 , 17 , 18 ]. Despite these multiple mechanisms of action, the therapeutic benefits of UDCA remain to be improved.…”

Section: Introductionmentioning

confidence: 99%

Omega-3 Polyunsaturated Fatty Acid: A Pharmaco-Nutraceutical Approach to Improve the Responsiveness to Ursodeoxycholic Acid

et al. 2021

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Ursodeoxycholic acid (UDCA) is the first line therapy for the treatment of cholestatic and autoimmune liver diseases. Its clinical use is currently limited by a significant proportion of non-responder patients. Polyunsaturated fatty acids (n-3 PUFAs) possess important anti-inflammatory properties and protect liver cells against bile acid (BA)-induced toxicity. The present study was designed to rapidly evaluate whether combining n-3 PUFAs (i.e., eicosapentaenoic [EPA] and docosahexaenoic [DHA] acids) to UDCA would provide additional benefits when compared to the drug alone. The parameters evaluated were (i) the expression of genes governing BA synthesis, transport, and metabolism; (ii) the prevention of BA-induced apoptosis and endoplasmic reticulum (ER)-stress; and (iii) the control of BA- and LPS-dependent inflammation. In the absence of n-3 PUFAs, most of the parameters investigated were unaffected by UDCA or were only altered by the higher dose (500 µM) of the drug. By contrast, in the presence of EPA/DHA (50/50 µM), all parameters showed a strongly improved response and the lowest UDCA dosage (50 µM) provided equal or better benefits than the highest dose used alone. For example, the combination EPA/DHA + UDCA 50 µM caused comparable down-regulation of the CYP7A1 gene expression and of the BA-induced caspase 3 activity as observed with UDCA 500 µM. In conclusion, these results suggest that the addition of n-3 PUFAs to UDCA may improve the response to the drug, and that such a pharmaco-nutraceutical approach could be used in clinic to open the narrow therapeutic dose of UDCA in cholestatic liver diseases.

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“…Clinically, the sICAM-1 is released into circulation at sites of in ammation or infection (22), and its serum level has been used as a marker of in ammatory and immune activity (23). It is hypothesized that the induction of ICAM-1 molecules in tumor cells leads to an increase in the cytotoxicity response, because there is an increase in antigen recognition (24,25).…”

Section: Discussionmentioning

confidence: 99%

Biological Implications of Circulating Soluble Intercellular Adhesion Molecule-1 in Colorectal Cancer Patients

Araki

Miki²,

Kusunoki³

2001

Scandinavian Journal of Gastroenterology

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Soluble intercellular adhesion molecule-1 in primary biliary cirrhosis: effect of ursodeoxycholic acid and immunosuppressive therapy

Cited by 7 publications

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Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications

Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications

Omega-3 Polyunsaturated Fatty Acid: A Pharmaco-Nutraceutical Approach to Improve the Responsiveness to Ursodeoxycholic Acid

Biological Implications of Circulating Soluble Intercellular Adhesion Molecule-1 in Colorectal Cancer Patients

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