Activation of mast cells by bile acids

Quist, Richard G.; Ton‐Nu, Huong‐Thu; Lillienau, Jan; Hofmann, Alan F.; Barrett, Kim E.

doi:10.1016/0016-5085(91)90024-f

Cited by 144 publications

(86 citation statements)

References 35 publications

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“…58 In support of this, it has been shown that in nephritic diseases exposure to cromolyn sodium decreases the incidences of pruritus. 59 Further, it has been shown that bile acids (that increase in content during liver disease) can regulate mast cell histamine release 60 and may also be a source of increased pruritus. 61,62 This suggests that manipulation of mast cell histamine by cromolyn sodium or bile acid therapy might also be an option for patients suffering from cholangiopathies or other liver diseases.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of mast cell-derived histamine secretion by cromolyn sodium treatment decreases biliary hyperplasia in cholestatic rodents

Kennedy

Hargrove

Graf

et al. 2014

Laboratory Investigation

143

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Cholangiopathies are characterized by dysregulation of the balance between biliary growth and loss. We have shown that histamine (HA) stimulates biliary growth via autocrine mechanisms. To evaluate the paracrine effects of mast cell (MC) stabilization on biliary proliferation, sham or BDL rats were treated by IP-implanted osmotic pumps filled with saline or cromolyn sodium (24 mg/kg BW/day (inhibits MC histamine release)) for 1 week. Serum, liver blocks and cholangiocytes were collected. Histidine decarboxylase (HDC) expression was measured using real-time PCR in cholangiocytes. Intrahepatic bile duct mass (IBDM) was evaluated by IHC for CK-19. MC number was determined using toluidine blue staining and correlated to IBDM. Proliferation was evaluated by PCNA expression in liver sections and purified cholangiocytes. We assessed apoptosis using real-time PCR and IHC for BAX. Expression of MC stem factor receptor, c-kit, and the proteases chymase and tryptase were measured by real-time PCR. HA levels were measured in serum by EIA. In vitro, MCs and cholangiocytes were treated with 0.1% BSA (basal) or cromolyn (25 mM) for up to 48 h prior to assessing HDC expression, HA levels and chymase and tryptase expression. Supernatants from MCs treated with or without cromolyn were added to cholangiocytes before measuring (i) proliferation by MTT assays, (ii) HDC gene expression by real-time PCR and (iii) HA release by EIA. In vivo, cromolyn treatment decreased BDL-induced: (i) IBDM, MC number, and biliary proliferation; (ii) HDC and MC marker expression; and (iii) HA levels. Cromolyn treatment increased cholangiocyte apoptosis. In vitro, cromolyn decreased HA release and chymase and tryptase expression in MCs but not in cholangiocytes. Cromolyn-treated MC supernatants decreased biliary proliferation and HA release. These studies provide evidence that MC histamine is key to biliary proliferation and may be a therapeutic target for the treatment of cholangiopathies.

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Section: Discussionmentioning

confidence: 99%

Inhibition of mast cell-derived histamine secretion by cromolyn sodium treatment decreases biliary hyperplasia in cholestatic rodents

Kennedy

Hargrove

Graf

et al. 2014

Laboratory Investigation

143

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“…Hydrophobic bile acids are known to be potent mast cell activators. 28,29 In PBC, concomitant increases in mast cell and eosinophil infiltration of portal tracts have been observed. 7 It has been postulated that the hepatic eosinophil hyperplasia in PBC is mediated by mast cells, in which activation by bile acids results in their releasing eosinophil-activating and -recruiting factors.…”

Section: Discussionmentioning

confidence: 99%

Mast cell hyperplasia in chronic rejection after liver transplantation

O'Keeffe¹

2002

Liver Transplantation

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The pathogenesis of chronic hepatic allograft rejection is poorly understood. Recent studies suggested that hepatic mast cells may be involved in the pathogenesis of chronic cholestatic liver disease. Because chronic rejection after liver transplantation is predominantly a cholestatic process, the aim of this study is to determine whether hepatic mast cells are involved in its pathogenesis. Biopsy specimens from (1) normal livers (n ‫؍‬ 5), (2) transplanted livers with end-stage chronic rejection (n ‫؍‬ 8), and (3) transplanted livers with acute cellular rejection (mild, n ‫؍‬ 7; moderate, n ‫؍‬ 5; severe, n ‫؍‬ 7) were studied. Biopsy specimens were stained immunohistochemically for mast cells with human antitryptase antibody. Mast cell density was significantly increased in the chronic-rejection group (4.9 ؎ 0.6/mm 2 ) compared with controls (2.9 ؎ 0.5/ mm 2 ; P < .05). The percentage of portal tracts containing mast cells was significantly greater in chronic-rejection (89% ؎ 8%) than control biopsy specimens (69% ؎ 5%; P < .

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“…Mast cells have also been involved in this process [98] . Indeed, BAs have been shown to induce prostaglandin [107] and histamine secretion [108] in vitro. Some of these actions may be secondary to direct mucosal injury [100,109] .…”

Section: Effect Of Ba On Ion Transportmentioning

confidence: 99%

Intestinal bile acid physiology and pathophysiology

Martínez‐Augustin¹,

Medina²

2008

WJG

138

114

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Bile acids (BAs) have a long established role in fat digestion in the intestine by acting as tensioactives, due to their amphipathic characteristics. BAs are reabsorbed very efficiently by the intestinal epithelium and recycled back to the liver via transport mechanisms that have been largely elucidated. The transport and synthesis of BAs are tightly regulated in part by specific plasma membrane receptors and nuclear receptors. In addition to their primary effect, BAs have been claimed to play a role in gastrointestinal cancer, intestinal inflammation and intestinal ionic transport. BAs are not equivalent in any of these biological activities, and structural requirements have been generally identified. In particular, some BAs may be useful for cancer chemoprevention and perhaps in inflammatory bowel disease, although further research is necessary in this field. This review covers the most recent developments in these aspects of BA intestinal biology.

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Activation of mast cells by bile acids

Cited by 144 publications

References 35 publications

Inhibition of mast cell-derived histamine secretion by cromolyn sodium treatment decreases biliary hyperplasia in cholestatic rodents

Inhibition of mast cell-derived histamine secretion by cromolyn sodium treatment decreases biliary hyperplasia in cholestatic rodents

Mast cell hyperplasia in chronic rejection after liver transplantation

Intestinal bile acid physiology and pathophysiology

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