Platelet-Activating Factor, a Critical Mediator in the Pathogenesis of Dextran Sulfate Sodium-Induced Colitis in Rats

Hirayama, Kazuhisa; Yokoi, Yoshihiro; Sakaguchi, Takanori; Nakamura, Toshio; Kashiwabara, Hidefumi; Sunayama, Kenichi

doi:10.1007/s10350-004-6503-7

Cited by 4 publications

(3 citation statements)

References 47 publications

(58 reference statements)

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“…It is possible, for example, that these differences in LTA structure could contribute to variability in bacterial uptake across the plasma membrane. Moreover, several studies suggest that PAFr may also mediate the recruitment of neutrophils and macrophages to the sites of inflammation and infection (Wallace, 1988; Hirayama et al , 2003; Han et al , 2006). Antagonistic blocking of the PAFr receptor has been shown to reduce the translocation of heat killed bacteria across Caco-2 monolayers and an M-cell coculture model (Tirer et al , 2006).…”

Section: Discussionmentioning

confidence: 99%

“…PAFr has been shown to be a pathway for nasopharyngeal passage of pneumococci (Cundell et al , 1995) and has been involved the transcytosis of pneumococci through brain microvascular endothelial cells (Ring et al , 1998). More recently PAFr has been implicated in inflammatory response during pneumococcal pneumonia and colitis (Hirayama et al , 2003; Rijneveld et al , 2004). In this study, we show that PAFr facilitates Gram-positive E.…”

Section: Discussionmentioning

confidence: 99%

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Hypoxia-inducible Factor-dependent Regulation of Platelet-activating Factor Receptor as a Route for Gram-Positive Bacterial Translocation across Epithelia

Keely

Glover

Weissmueller

et al. 2010

MBoC

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hypoxia-inducible Factor-dependent Regulation of Platelet-activating Factor Receptor as a Route for Gram-Positive Bacterial Translocation across Epithelia

Keely

Glover

Weissmueller

et al. 2010

MBoC

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“…Indeed, there was a marked production of TNF‐ α and IL‐1 β after injection of PAF in the rat paw. These results are consistent with others showing that cytokine synthesis induced in models of pulmonary infection with Gram‐negative bacteria and colitis is broadly dependent on PAF ( Soares et al ., 2002 ; Galvez et al ., 2003 ; Hirayama et al ., 2003 ; Souza et al ., 2003 ; Ferreira et al ., 2004 ). Whereas TNF‐ α peaked at 1 h after PAF injection, levels of IL‐1 β were elevated at 3 and 6 h after PAF.…”

Section: Discussionmentioning

confidence: 99%

Cytokines and neutrophils as important mediators of platelet‐activating factor‐induced kinin B₁ receptor expression

Fernandes¹,

Passos²,

Campos³

et al. 2005

British J Pharmacology

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1 PAF injection into the rat paw is accompanied by the concomitant activation of NF-kB and neutrophil influx, which appears to be relevant to the up-regulation of kinin B 1 receptors. Herein, we analyse the role of TNF-a and IL-1b production for PAF-induced B 1 receptor upregulation in the rat paw. Additionally, we evaluate how cytokine production and neutrophil migration fit into the temporal sequence of events leading to PAF-induced B 1 receptor upregulation. 2 In our experiments, treatment with PAF resulted in a marked increase of B 1 receptor-mediated paw oedema and in situ production of TNF-a at 1 h and IL-1b at 3 and 6 h later. B 1 receptor-mediated paw oedema was significantly inhibited by anti-TNF-a antibody and by interleukin-1 receptor antagonist (IRA). 3 TNF-a was necessary for the local PAF-induced IL-1b production. NF-kB blocker PDTC prevented the production of both TNF-a and IL-1b, indicating that cytokine production is NF-kB dependent. 4 Depletion of neutrophils with an anti-PMN antibody prevented IL-1b, but not TNF-a, production. Although both TNF-a and IL-1b are relevant to functional B 1 receptor upregulation, PAF-induced increase in B 1 receptor mRNA was markedly suppressed by anti-TNF-a and, to a lesser extent, by IRA. B 1 receptor mRNA expression was also prevented by the anti-PMN antibody. 5 In conclusion, the activation of the TNF-a/neutrophil axis by PAF seems to be sufficient for B 1 receptor mRNA production. However, the TNF-a/neutrophil axis is also necessary for IL-1b production. These two processes might lead to the appearance of functional kinin B 1 upregulation receptors in vivo after PAF treatment.

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Pancreatic and mucosal enzymes in choline phospholipid digestion

Nilsson

Duan

2019

American Journal of Physiology-Gastrointestinal and Liver Physi

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The digestion of choline phospholipids is important for choline homeostasis, lipid signaling, postprandial lipid and energy metabolism, and interaction with intestinal bacteria. The digestion is mediated by the combined action of pancreatic and mucosal enzymes. In the proximal small intestine, hydrolysis of phosphatidylcholine (PC) to 1-lyso-PC and free fatty acid (FFA) by the pancreatic phospholipase A2 IB coincides with the digestion of the dietary triacylglycerols by lipases, but part of the PC digestion is extended and must be mediated by other enzymes as the jejunoileal brush-border phospholipase B/lipase and mucosal secreted phospholipase A2 X. Absorbed 1-lyso-PC is partitioned in the mucosal cells between degradation and reacylation into chyle PC. Reutilization of choline for hepatic bile PC synthesis, and the reacylation of 1-lyso-PC into chylomicron PC by the lyso-PC-acyl-CoA-acyltransferase 3 are important features of choline recycling and postprandial lipid metabolism. The role of mucosal enzymes is emphasized by sphingomyelin (SM) being sequentially hydrolyzed by brush-border alkaline sphingomyelinase (alk-SMase) and neutral ceramidase to sphingosine and FFA, which are well absorbed. Ceramide and sphingosine-1-phosphate are generated and are both metabolic intermediates and important lipid messengers. Alk-SMase has anti-inflammatory effects that counteract gut inflammation and tumorigenesis. These may be mediated by multiple mechanisms including generation of sphingolipid metabolites and suppression of autotaxin induction and lyso-phosphatidic acid formation. Here we summarize current knowledge on the roles of pancreatic and mucosal enzymes in PC and SM digestion, and its implications in intestinal and liver diseases, bacterial choline metabolism in the gut, and cholesterol absorption.

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Platelet-Activating Factor, a Critical Mediator in the Pathogenesis of Dextran Sulfate Sodium-Induced Colitis in Rats

Cited by 4 publications

References 47 publications

Hypoxia-inducible Factor-dependent Regulation of Platelet-activating Factor Receptor as a Route for Gram-Positive Bacterial Translocation across Epithelia

Hypoxia-inducible Factor-dependent Regulation of Platelet-activating Factor Receptor as a Route for Gram-Positive Bacterial Translocation across Epithelia

Cytokines and neutrophils as important mediators of platelet‐activating factor‐induced kinin B₁ receptor expression

Pancreatic and mucosal enzymes in choline phospholipid digestion

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Platelet-Activating Factor, a Critical Mediator in the Pathogenesis of Dextran Sulfate Sodium-Induced Colitis in Rats

Cited by 4 publications

References 47 publications

Hypoxia-inducible Factor-dependent Regulation of Platelet-activating Factor Receptor as a Route for Gram-Positive Bacterial Translocation across Epithelia

Hypoxia-inducible Factor-dependent Regulation of Platelet-activating Factor Receptor as a Route for Gram-Positive Bacterial Translocation across Epithelia

Cytokines and neutrophils as important mediators of platelet‐activating factor‐induced kinin B1 receptor expression

Pancreatic and mucosal enzymes in choline phospholipid digestion

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Cytokines and neutrophils as important mediators of platelet‐activating factor‐induced kinin B₁ receptor expression