PAF-acether and acetylhydrolase in stool of patients with Crohn's disease

Denizot, Yves; Chaussade, Stanislas; Nathan, Nathalie; Colombel, Jean–Frédéric; Bossant, Marie‐Jeanne; Cherouki, N.; Benveniste, J.; Couturier, Daniel

doi:10.1007/bf01307739

Cited by 51 publications

(16 citation statements)

References 20 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] .…”

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

confidence: 80%

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: 80%

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

He¹

2004

WJG

227

173

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“…PAF has been measured in the stool of adult patients with a variety of gastrointestinal diseases, including pouchitis [21], Crohn's disease [22,23], ulcerative colitis [24] and infectious diarrhea [25] and has been found to be significantly elevated in those conditions compared to levels in normal adult volunteers. Studies measuring stool PAF in infants are limited to a single report of 4 infants with hemorrhagic colitis [26].…”

Section: Discussionmentioning

confidence: 99%

Platelet-Activating Factor Concentration in the Stool of Human Newborns: Effects of Enteral Feeding and Neonatal Necrotizing Enterocolitis

Amer¹,

Hedlund²,

Rochester³

et al. 2004

Neonatology

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Epidemiologic studies have identified enteral feedings as a risk factor for necrotizing enterocolitis (NEC). Enteral feedings provide the substrate for colonization of the newborn gut with gram-negative bacteria with endotoxin production, which may trigger the production of endogenous inflammatory mediators, including platelet-activating factor (PAF). In this prospective study, we examined the effect of enteral feeding on PAF concentration in the stool of preterm and full-term human newborns. The concentration of PAF levels in stool was measured at the following times: at passage of first meconium, within 24 h prior to the onset of feedings, at the 3rd and 14th day of feeding and at any time confirmed NEC developed. Stool samples also were analyzed for levels of acetylhydrolase, the PAF breakdown enzyme. Stool PAF concentration rose significantly following the start of enteral feedings. The mean PAF concentration for day 14 samples was significantly higher than the mean concentration of meconium samples (4.90 ± 1.03 vs. 1.81 ± 0.38 ng/g, p < 0.05) and day 0 samples (4.90 ± 1.03 vs. 1.79 ± 0.39 ng/g, p < 0.05). For the 7 patients diagnosed with definite NEC, the mean stool PAF concentration was 12.42 ± 0.77 ng/g, significantly elevated compared to the mean PAF levels in stool from healthy infants at all sampling times (p < 0.01). There was no significant change in acetylhydrolase activity at any of the sampling times. Stool PAF concentration increases with the provision of enteral feedings and rises further with the development of NEC. Since stool acetylhydrolase activity remained unchanged, we speculate the increase of PAF in stool likely represents increased PAF production at the local level following the provision of enteral feedings or the development of neonatal necrotizing enterocolitis.

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“…The stomach and the small intestine are severely affected while the colon is apparently unaffected (Wallace and Whittle 1986). PAF is also elevated in the mucosa or stool of patients with inflammatory bowel disease (Sobhani et al 1992;Denizot et al 1992;Eliakim et al 1988) and in animal models of intestinal inflammation (Rachmilewitz et al 1990;MacNaughton et al 1992). Administration of castor oil (Pinto et al 1989), diphenylmethane derivatives (Izzo et al 1993) or endotoxin ) produces diarrhoea and gastrointestinal damage that is associated with the increased formation of PAF throughout the digestive tract.…”

Section: Introductionmentioning

confidence: 99%

Relationship between nitric oxide and platelet-activating factor in castor-oil induced mucosal injury in the rat duodenum

Mascolo

Izzo

Gaginella

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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The modulation of platelet activating factor (PAF) formation in duodenal tissue by nitric oxide (NO) released in response to castor oil was studied in rats pretreated with NG-nitro-L-arginine methyl ester (L-NAME, 6.25-25 mg/kg, i.p.), an inhibitor of NO synthase, NG-nitro-D-arginine methyl ester (D-NAME, 25 mg/kg, i.p.), the inactive enantiomer of L-NAME or isosorbide-5-mononitrate (IMN, 30-90 mg/kg, p.o.), a NO donating compound. Castor oil (2 ml/rat orally) increased PAF production in the rat duodenum 3 h after challenge. L-NAME, but not D-NAME, enhanced the amount of PAF formed by duodenal tissue, while IMN (30-90 mg/kg) counteracted the effects of L-NAME (12.5 mg/kg) and also reduced PAF release in the tissue of rats treated with castor oil. L-NAME 12.5 mg/kg, but not D-NAME, enhanced both macroscopic damage and acid phosphatase release induced by castor oil. These effects were reduced by a PAF antagonist BN 52021 (3-t-Butyl-hexahydro-4, 7b, 11-trihydroxy-8-methyl-9H-1, 7a-epoxymethano-1H, 6aH-cyclopenta [c] furo [2, 3b] furo [3'2':3,4] cyclopenta [1.2-d]furan-5,9,12(4H)trione) 10 and 20 mg/kg i.p. Such findings suggest that endogenous nitric oxide could reduce PAF biosynthesis in castor oil-treated rats.

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PAF-acether and acetylhydrolase in stool of patients with Crohn's disease

Cited by 51 publications

References 20 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 Concentration in the Stool of Human Newborns: Effects of Enteral Feeding and Neonatal Necrotizing Enterocolitis

Relationship between nitric oxide and platelet-activating factor in castor-oil induced mucosal injury in the rat duodenum

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