Raised concentrations of platelet activating factor in colonic mucosa of Crohn's disease patients.

Sobhani, Iradj; Hochlaf, S.; Denizot, Yves; Vissuzaine, C; René, E; Benveniste, J.; Lewin, M. M. J.; Mignon, M

doi:10.1136/gut.33.9.1220

Cited by 55 publications

(28 citation statements)

References 28 publications

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“…The increased secretion of PAF was detected in the stool of patients with active Crohn's disease, but not in that of patients with irritable bowel syndrome [140] . The level of PAF was also higher in colonic mucosa of patients with Crohn's disease than in colonic mucosa of healthy controls [141] . These indicated that PAF might be involved in the pathogenesis of Crohn's disease [142] .…”

Section: Involvement Of Pgd2 Ltc4 and Paf In Pathogenesis Of Ibdmentioning

confidence: 83%

Key role of mast cells and their major secretory products in inflammatory bowel disease

He¹

2004

WJG

227

173

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Historically, mast cells were known as a key cell type involved in type I hypersensitivity. Until last two decades, this cell type was recognized to be widely involved in a number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers of mast cells were observed in the mucosa of the ileum and colon of patients with IBD, which was accompanied by great changes of the content in mast cells such as dramatically increased expression of TNFα, IL-16 and substance P. The evidence of mast cell degranulation was found in the wall of intestine from patients with IBD with immunohistochemistry technique. The highly elevated histamine and tryptase levels were detected in mucosa of patients with IBD, strongly suggesting that mast cell degranulation is involved in the pathogenesis of IBD. However, little is known of the actions of histamine, tryptase, chymase and carboxypeptidase in IBD. Over the last decade, heparin has been used to treat IBD in clinical practice. The low molecular weight heparin (LMWH) was effective as adjuvant therapy, and the patients showed good clinical and laboratory response with no serious adverse effects. The roles of PGD2, LTC4, PAF and mast cell cytokines in IBD were also discussed. Recently, a series of experiments with dispersed colon mast cells suggested there should be at least two pathways in man for mast cells to amplify their own activationdegranulation signals in an autocrine or paracrine manner. The hypothesis is that mast cell secretogogues induce mast cell degranulation, release histamine, then stimulate the adjacent mast cells or positively feedback to further stimulate its host mast cells through H 1 receptor. Whereas released tryptase acts similarly to histamine, but activates mast cells through its receptor PAR-2. The connections between current anti-IBD therapies or potential therapies for IBD with mast cells were discussed, implicating further that mast cell is a key cell type that is involved in the pathogenesis of IBD. In conclusion, while pathogenesis of IBD remains unclear, the key role of mast cells in this group of diseases demonstrated in the current review implicates strongly that IBD is a mast cell associated disease. Therefore, close attentions should be paid to the role of mast cells in IBD.He SH. Key role of mast cells and their major secretory products in inflammatory bowel disease.

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Section: Involvement Of Pgd2 Ltc4 and Paf In Pathogenesis Of Ibdmentioning

confidence: 83%

Key role of mast cells and their major secretory products in inflammatory bowel disease

He¹

2004

WJG

227

173

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“…PAF interacts with a G protein-linked receptor protein (PAFR) cloned from guinea pig lung (Honda et al, 1991), rat spleen (Bito et al, 1994), human heart (Sugimoto et al, 1992), HL60 cells (Ye et al, 1991), and U937 cells (Kunz et al, 1992) and expressed at low-levels in central nervous system (CNS) (Bito et al, 1994). PAF regulates peripheral cytokine and inflammatory networks (Bonavida and MenciaHuerta, 1994) with prolonged signal transduction implicated in the pathogenesis of hypotensive shock, bronchial asthma, ulcerative colitis, Crohn's disease, and tumour progression (Sobhani et al, 1992;Yamamoto et al, 1993;Ferraris et al, 1993;Bennett et al, 1993;Graham et al, 1994). In CNS, sustained PAF stimulation is observed during ischemia, encephalitis, meningitis, and human immunodeficiency virus-1 infection (Kumar et al, 1988;Gelbard et al, 1994;Marcheselli and Bazan, 1994).…”

Section: Introductionmentioning

confidence: 99%

Platelet activating factor receptor expression is associated with neuronal apoptosis in an in vivo model of excitotoxicity

et al. 1998

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Platelet activating factor (PAF), an endogenous proinflammatory agent, mediates neuronal survival, glutamate release, and transcriptional activation following excitotoxin challenge. To determine whether PAF receptor (PAFR) expression is altered during excitotoxicity, changes in PAFR mRNA localization were compared with markers of neuronal apoptosis and reactive gliosis following systemic injection of kainic acid. Data from semi-quantitative RT-PCR, in situ hybridization, DNA fragmentation, cellular morphology analysis, and immunohistochemistry demonstrate that the localization of PAFR mRNA is altered during kainic acid-induced neurodegeneration. While PAFR mRNA is normally exhibited by neurons and microglia in rat hippocampus, expression becomes restricted to apoptotic neurons and to glia involved in phagocytosing apoptotic debris following treatment with excitotoxin. PAFR mRNA is rarely detected in surviving neurons. These data provide the first indication that PAFRexpressing neurons may be preferentially susceptible to excitotoxic challenge.

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“…If the basolateral loading mechanisms are stimulated as well, the result is transepithelial transport, and if they are not, the result is net loss of Cl Ϫ and/or bicarbonate. Clinical studies suggest that stool PAF levels can correlate with patients at risk for IBD and disease severity and that serum PAF levels can correlate with disease severity in NEC (38,39,45). If PAF is a critical molecule in the pathogenesis of IBD, and if an early effect is induced intracellular acidosis, inhibition of this effect may lead to a potential therapy for a subset of patients at risk for IBD due to elevated PAF levels.…”

Section: Discussionmentioning

confidence: 99%

“…However, the mechanism of PAF-induced intestinal injury is incompletely understood. It is known that tissue and/or serum PAF levels are elevated in patients with Crohn's disease, ulcerative colitis, and neonatal necrotizing enterocolitis (NEC), and levels appear to correlate with disease severity (13,26,39,45). In animal models of NEC, PAF receptor blockade or administration of the PAF-degrading enzyme PAF acetylhydrolase reduced the incidence of experimental NEC (7,9).…”

mentioning

confidence: 99%

Platelet-activating factor-induced chloride channel activation is associated with intracellular acidosis and apoptosis of intestinal epithelial cells

Claud

Lü²,

Wang³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Raised concentrations of platelet activating factor in colonic mucosa of Crohn's disease patients.

Cited by 55 publications

References 28 publications

Key role of mast cells and their major secretory products in inflammatory bowel disease

Key role of mast cells and their major secretory products in inflammatory bowel disease

Platelet activating factor receptor expression is associated with neuronal apoptosis in an in vivo model of excitotoxicity

Platelet-activating factor-induced chloride channel activation is associated with intracellular acidosis and apoptosis of intestinal epithelial cells

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