2000
DOI: 10.1002/hep.510310120
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Abstract: In inflammatory disease states, such as hepatitis and sepsis, cholestasis is a common observation. 1,2 Although it is known that endotoxemia decreases hepatocellular bile acid uptake in vivo, the sequence of events leading to impairment of transport for bile salts is incompletely understood. The role of macrophages as mediators in endotoxemia or exposure of the liver to toxins such as alcohol or D-galactosamine, in particular through the release of proinflammatory cytokines, has been the focus of recent studie… Show more

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Cited by 25 publications
(19 citation statements)
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“…It is generally accepted that SLTs causes HUS in humans and animals through damage to the vascular endothelial vessels by cytokines (5,14), due to up-regulation of the expression of Gb 3 receptor in endothelial cells (20), suggesting that cytokines play a central role in SLT-II-induced histopathological lesions. On the other hand, cytokines such as TNF-␣, interleukin-1␤ (IL-1␤), and IL-6 play an important role in the regulation of hepatic transporters (2,33). It was recently reported that SLT-II overproduces TNF-␣ in plasma and that PTX partly ameliorates SLT-II-induced reductions in kidney and brain functions (42,43).…”
Section: Discussionmentioning
confidence: 99%
“…It is generally accepted that SLTs causes HUS in humans and animals through damage to the vascular endothelial vessels by cytokines (5,14), due to up-regulation of the expression of Gb 3 receptor in endothelial cells (20), suggesting that cytokines play a central role in SLT-II-induced histopathological lesions. On the other hand, cytokines such as TNF-␣, interleukin-1␤ (IL-1␤), and IL-6 play an important role in the regulation of hepatic transporters (2,33). It was recently reported that SLT-II overproduces TNF-␣ in plasma and that PTX partly ameliorates SLT-II-induced reductions in kidney and brain functions (42,43).…”
Section: Discussionmentioning
confidence: 99%
“…[18][19][20][21][22][23][24][25][26] Mrp2 is one of the important hepatocyte transport proteins and mediates ATP-dependent canalicular excretion of a wide range of amphipathic anionic substances. [27][28] However, it has not been known how mrp2 is involved in the cholestasis associated with TNB-induced colitis.…”
Section: Discussionmentioning
confidence: 99%
“…17 Impaired functions and decreased expressions of specific hepatocellular transport proteins have been implicated in the pathogenesis of cholestasis. [18][19][20][21][22][23][24][25][26] These abnormalities explain …”
mentioning
confidence: 99%
“…APR leads to the pathogenesis and progression of a variety of liver diseases, including cholestasis, which results from altered expression of the bile acid transporters, including sodium/taurocholate cotransporter (Ntcp/Slc10a1), bile acid salt exporter pump (Bsep, Abcb11), and the multi-drug resistance-related proteins (Mrp, Abcc) 2 & 3 [2,5]. The effects of LPS on hepatic genes are attenuated in rodent models upon inactivation or depletion of KCs, or by administration of anti-cytokine antibodies [6][7][8][9]. This suggests that counteracting either the production or intracellular action of inflammatory mediators secreted by KCs may attenuate the pathogenesis of inflammation in liver diseases.…”
Section: Introductionmentioning
confidence: 99%