Cytokine- and calcium ionophore A23187-mediated arachidonic acid metabolism in neutrophils

Ulich, Thomas R.; Busser, Katie; Longmuir, Kenneth J.

doi:10.1016/1043-4666(90)90029-s

Cited by 5 publications

(4 citation statements)

References 25 publications

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“…Arachidonic acid in turn can be converted into eicosanoids by lipoxygenase and cyclooxygenase pathways, thus linking interleukin production with the synthesis of eicosanoids during inflammatory states. 19 Our results indicate that CACO-2 cells release significant amounts of PGE2 in response to stimulation with either LPS or IL-I, suggesting that these stimulants have the capacity to directly regulate the synthesis of prostanoids in these cells. Since LTB4 levels were not enhanced under these same conditions, these data further suggest that either the lipoxygenase arm of the arachidonic acid cascade does not respond in a similar manner to these same agonists, or more likely that the noted increases in PGE2 can exhibit an inhibitory effect on LTB4…”

Section: Discussionmentioning

confidence: 58%

The effect of an interleukin receptor antagonist (IL‐1ra) on colonocyte eicosanoid release

Smith

Rieckenberg

Longo

et al. 1996

Mediators of Inflammation

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We investigated whether an interleukin 1 receptor antagonist (IL-1ra) altered cellular release of prostanoids and leukotrienes in a transformed colonic cell line (CACO-2) in the presence of proinflammatory stimuli. Cellular inflammation was induced by treatment with lipopolysaccharide (LPS) or the cytokine, interleukin 1 beta (IL-1β). In a separate set of experiments, cells were pretreated with IL-1ra prior to exposure to LPS or IL-1β. Prostaglandin E2 and leukotriene B4 (LTB4) levels were quantified by ELISA assays. Both LPS and IL-1β exposure were noted to stimulate cellular PGE2 release, a response which was significantly inhibited by IL-1ra treatment. Either stimulant when administered alone failed to stimulate release of LTB4. When administered after IL-1ra pretreatment however, both stimuli caused a significant increase in LTB4 release. These results suggest that a cytokine receptor antagonist can selectively influence eicosanoid production in this cell line. Furthermore, this study suggests that a IL-1ra may have a future clinical role in the treatment of inflammatory disorders of the colon which are intimately linked to enhanced eicosanoid synthesis.

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Section: Discussionmentioning

confidence: 58%

The effect of an interleukin receptor antagonist (IL‐1ra) on colonocyte eicosanoid release

Smith

Rieckenberg

Longo

et al. 1996

Mediators of Inflammation

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“…The prompt release of arachidonic acid from plasma membrane phospholipids is an event which may represent the receptor-mediated activation of membrane phospholipases and that may contribute to the priming of the cells for enhancement of their functional responsiveness (Sullivan et al 1987). However, it was determined in another study that GM-CSF is unable to induce the release of cell-incorporated arachidonic acid or to increase the level of phosphatidic acid directly (Ulich et al 1990a).…”

Section: E Synthesis Of Mediators and Enzymesmentioning

confidence: 99%

Immunomodulation by colony-stimulating factors

Hartung

1999

Reviews of Physiology, Biochemistry and Pharmacology

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“…Deposition of IgA1-containing immune complexes in the glomerular mesangium results in glomerular and tubulointerstitial injury via activation of inflammatory cascade by the secretion of various proinflammatory and profibrotic cytokines . It is well known that proinflammatory cytokines can stimulate the release of arachidonic acid (ARA) from the cell membrane and the metabolism of ARA thereafter because multiple metabolism enzymes of ARA are inducible. , In return, the many metabolites of ARA, such as prostaglandins (PGs), leukotrienes (LTs), and epoxyeicosatrienoic acids (EETs), have crucial roles in the manipulation of inflammation. − To this end, we hypothesize that the metabolism of ARA plays an important role in the pathogenesis of IgAN. However, the role of ARA metabolism in the pathogenesis of IgAN remains largely unknown so far, although human and murine renal glomeruli were previously reported to metabolize the ARA in vitro …”

Section: Introductionmentioning

confidence: 99%

“…1 It is well known that proinflammatory cytokines can stimulate the release of arachidonic acid (ARA) from the cell membrane and the metabolism of ARA thereafter because multiple metabolism enzymes of ARA are inducible. 6,7 In return, the many metabolites of ARA, such as prostaglandins (PGs), leukotrienes (LTs), and epoxyeicosatrienoic acids (EETs), have crucial roles in the manipulation of inflammation. 8−10 To this end, we hypothesize that the metabolism of ARA plays an important role in the pathogenesis of IgAN.…”

Section: ■ Introductionmentioning

confidence: 99%

Targeted Metabolomics Study of Human Plasma Revealed Activation of the Cytochrome P450 Epoxygenase/Epoxide Hydrolase Axis in Patients with IgA Nephropathy

Deng

et al. 2022

J. Proteome Res.

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IgA nephropathy (IgAN) is the most common primary glomerulonephritis and a leading cause of chronic kidney disease. The pathogenic mechanism of IgAN remains largely unknown and thus a specific therapeutic target is lacking. Here, we reported that the cytochrome P450 (CYP) epoxygenase/epoxide hydrolase (EH) axis was activated in the patients and is likely a therapeutic target for IgAN. Specifically, quantitative profiling of the plasma from IgAN patients and healthy controls revealed significant changes in plasma levels of CYP/EH-mediated lipid epoxides and diols. Subsequently, CYP2C8, CYP2C18, CYP2J2, EPHX1, and EPHX2 were found to be significantly increased in whole blood cells at mRNA levels from the IgAN patients when compared with those of healthy controls. Immunohistochemical analysis showed that all five CYPs and two EHs were upregulated in the kidney tissue from IgAN patients when compared with normative renal tissue, but the expression locations of the proteins were different with most of them. Treatment of HK-2 cells with IgA1 increased cell viability, compressed cell apoptosis, and increased the protein levels of CYP2C9, EPHX1, and EPHX2. All the results agreed that CYPs/EHs axis is likely the prophylactic and therapeutic target for IgAN, providing IgAN patients with a new intervention strategy.

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Cytokine- and calcium ionophore A23187-mediated arachidonic acid metabolism in neutrophils

Cited by 5 publications

References 25 publications

The effect of an interleukin receptor antagonist (IL‐1ra) on colonocyte eicosanoid release

The effect of an interleukin receptor antagonist (IL‐1ra) on colonocyte eicosanoid release

Immunomodulation by colony-stimulating factors

Targeted Metabolomics Study of Human Plasma Revealed Activation of the Cytochrome P450 Epoxygenase/Epoxide Hydrolase Axis in Patients with IgA Nephropathy

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