Studies of cellular mechanisms for the generation of superoxide by guinea-pig eosinophils and its dissociation from granule peroxidase release

Shute, Janis K.; Rimmer, S. J.; Akerman, C.; Church, Martin K.; Holgate, Stephen T.

doi:10.1016/0006-2952(90)90231-9

Cited by 18 publications

(15 citation statements)

References 49 publications

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“…It enhances eosinophil adherence to vascular endothelial cells (65). PAF activates immune as well as nonimmune cells and induces release of itself and other inflammatory mediators, including reactive oxygen species (ROS) (114,140). PAF is produced by and released from the esophageal mucosa after acid exposure (11) and it is increased in the circular muscle layer of feline esophagitis model and in chronic esophagitis in humans (14,16).…”

Section: Inflammatory Mediators In the Inflamed Esophageal Mucosamentioning

confidence: 99%

Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis

Rieder

Biancani

Harnett

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

111

102

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Gastroesophageal reflux disease (GERD) is one of the most common problems in clinical practice today. It is widely believed that functional and structural abnormalities of the gastroesophageal junction as well as an abnormal exposure to gastroduodenal contents are the main contributors to its pathogenesis. Novel findings of the inflammatory process in GERD suggest a far more complex process involving multifaceted inflammatory mechanisms. This review summarizes knowledge about the expression of inflammatory mediators in GERD and their potential cellular sources and provides an integrated concept of disease pathogenesis. In addition we evaluate the contribution of inflammatory mediators to well-known complications of GERD, namely motility abnormalities, fibrosis, and carcinogenesis. Novel findings regarding the pathophysiology of esophageal inflammation should enhance our understanding of GERD and its complications and provide new treatment insights.

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Section: Inflammatory Mediators In the Inflamed Esophageal Mucosamentioning

confidence: 99%

Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis

Rieder

Biancani

Harnett

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

111

102

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“…For example, PAF is an effective chemotactic factor for human eosinophils in vitro (5,6) and promotes eosinophil adherence to vascular endothelial cells through a ␤ 2 integrin, CD11b/CD18 (Mac-1) (7). Furthermore, in eosinophils PAF induces various effector functions, such as degranulation (8,9), production of superoxide anion (10,11) and leukotriene C4 (12,13), and formation of lipid bodies (14). Interestingly, PAF is generated by human eosinophils themselves and amplifies their effector functions in an autocrine manner (15).…”

Section: P Latelet-activating Factor (Paf)mentioning

confidence: 99%

Platelet-Activating Factor Activates Two Distinct Effector Pathways in Human Eosinophils

Katô

Kimura

Motegi

et al. 2002

The Journal of Immunology

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In granulocytes, platelet-activating factor (PAF) shares many of its biological effects with other chemotactic factors, such as FMLP, complement fragments, and lipid mediators. Two unique effects are that PAF is relatively resistant to pertussis toxin (PTX) and that PAF activates the inflammatory functions of eosinophils more strongly than it activates those of neutrophils. To investigate the molecular mechanisms of the responses of eosinophils to PAF, we analyzed superoxide anion production by a chemiluminescence method that provides real-time kinetic data for the cellular responses. We found that PAF induced bimodal superoxide anion production in human eosinophils, consisting of an intense, but transient, first phase and a larger and sustained second phase. In contrast, PAF induced essentially a transient unimodal response in human neutrophils. The two phases of eosinophil response were mediated by distinct cellular mechanisms: the second phase was highly dependent on cellular adhesion and β2 integrins, but the first phase was independent of both adhesion and β2 integrins. The upstream signaling mechanisms were also different: the second phase was mediated by PTX-resistant G-protein(s) and through activation of phosphatidylinositol 3-kinase, while the first phase was mediated by PTX-sensitive G-protein(s). Furthermore, the second-phase response was ∼100-fold more resistant to inhibition by a competitive PAF receptor antagonist than the first phase. Thus, eosinophils and neutrophils react differently to PAF, and PAF activates two separate and distinct effector pathways in human eosinophils. These two activation pathways may explain the eosinophils’ strong and diverse biological responses to PAF.

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“…PAF increases the binding of IgE to human eosinophils and enhances cytotoxicity towards schistosomula of Schistosoma mansoni [14]. Furthermore, PAF promotes actin polymerization [15]and eosinophil adherence to vascular endothelial cells through a β 2 integrin, αMβ2 (CD11b/CD18, Mac-1) [16]and evokes the release of granule proteins [17, 18], reactive oxygen species [19, 20], leukotriene (LT) C 4 [21], and formation of lipid bodies [22]. A recent report suggested that PAF induces the release of neurotrophin nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 [23], and matrix metalloproteinase-9 [24]in human eosinophils.…”

Section: Introductionmentioning

confidence: 99%

Dual Signaling and Effector Pathways Mediate Human Eosinophil Activation by Platelet-Activating Factor

Katô¹,

Kita²,

Tachibana³

et al. 2004

Int Arch Allergy Immunol

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Platelet-activating factor (PAF) induces various cellular functions in eosinophils including chemotaxis, adhesion, superoxide anion (O₂^–) production, and degranulation. While PAF shares many biological effects with other chemotactic factors such as N-formyl-methionyl-leucyl-phenylalanine, complement fragments, and lipid mediators, PAF is unique in that its action is relatively resistant to pertussis toxin (PTX), and in activating eosinophils more strongly than neutrophils. In this review we consider how PAF might activate human eosinophils in preference to neutrophils, and discuss possible mechanisms of PAF-induced activation of human eosinophils via two distinct signaling and effector pathways. Recently we analyzed O₂^– production by eosinophils using a sensitive, real-time chemiluminescence method. Our results showed that in human eosinophils PAF activates two distinct signaling and effector pathways coupled to the PAF receptor: one linked to PTX-sensitive G protein(s) and another to PTX-resistant G protein(s), phosphatidylinositol 3-kinase, and cellular adhesion. This activation of two different G proteins by the eosinophil PAF receptor may explain the strong and diverse biological responses of human eosinophils to PAF.

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Studies of cellular mechanisms for the generation of superoxide by guinea-pig eosinophils and its dissociation from granule peroxidase release

Cited by 18 publications

References 49 publications

Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis

Inflammatory mediators in gastroesophageal reflux disease: impact on esophageal motility, fibrosis, and carcinogenesis

Platelet-Activating Factor Activates Two Distinct Effector Pathways in Human Eosinophils

Dual Signaling and Effector Pathways Mediate Human Eosinophil Activation by Platelet-Activating Factor

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