The monocyte-derived neutrophil activating peptide (NAP/interleukin 8) stimulates human neutrophil arachidonate-5-lipoxygenase, but not the release of cellular arachidonate.

Schröder, Jens‐M.

doi:10.1084/jem.170.3.847

Cited by 162 publications

(77 citation statements)

References 40 publications

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“…4,27,35,[37][38][39] In addition to their roles in neutrophil recruitment, TNF␣, IL-1␤, and especially IL-8 promote neutrophil-mediated tissue injury by stimulating neutrophil degranulation and the extracellular release of arachidonic acid metabolites, toxic oxygen radicals, and proteolytic enzymes. 6,10,13,[28][29][30] Our findings indicate that IL-8 is the dominant inflammatory cytokine expressed within the lungs during the acute phase of BPP. Throughout the 24 hour period following inoculation of P. haemolytica, IL-8 was expressed in much greater quantities than either TNF␣ or IL-1␤.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Expression of Tumor Necrosis Factor Alpha, Interleukin-1 Beta, and Interleukin-8 in the Acute Phase of Bovine Pneumonic Pasteurellosis

et al. 2001

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Abstract. Inflammatory cytokines are suspected to contribute to the pathogenesis of bovine pneumonic pasteurellosis (BPP) through neutrophil recruitment, leukocyte activation, and the induction of a broad array of soluble inflammatory mediators. An in vivo experimental model of BPP was used to characterize the pulmonary expression kinetics of tumor necrosis factor alpha (TNF␣), interleukin-1 beta (IL-1␤), and interleukin-8 (IL-8) genes and proteins during the acute phase of disease development. Cytokine expression in bronchoalveolar lavage (BAL) fluid, BAL cells, and pneumonic lung parenchyma was quantitated by northern blot analysis, enzyme-linked immunosorbent assay (ELISA), and in situ hybridization at 2, 4, 8, 16, and 24 hours after endobronchial inoculation of Pasteurella (Mannheimia) haemolytica. Expression of TNF␣, IL-1␤, and IL-8 was significantly increased in the airways and lung lesions of infected calves as compared with mock-infected controls. Although kinetic patterns varied, peak levels of cytokine mRNA occurred within 8 hours postinfection (PI), and peak cytokine concentrations occurred within 16 hours PI. In all samples, IL-8 was expressed to the greatest extent and TNF␣ was least expressed. Expression of TNF␣ was restricted to alveolar macrophages. Alveolar and interstitial macrophages produced IL-1␤ and IL-8 in the first 4 hours; bronchial and bronchiolar epithelial cells were also significant sources of IL-8 during this period. By 8 hours PI, neutrophils were the dominant source of both IL-1␤ and IL-8. These findings demonstrate a spatial and temporal association between pulmonary expression of inflammatory cytokines and acute lung pathology, supporting the hypothesis that cytokines contribute to inflammatory lung injury in BPP.

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Section: Discussionmentioning

confidence: 99%

Pulmonary Expression of Tumor Necrosis Factor Alpha, Interleukin-1 Beta, and Interleukin-8 in the Acute Phase of Bovine Pneumonic Pasteurellosis

et al. 2001

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“…Such a direct effect assumes that binding of IL-8, or one of the other ELR ϩ chemokines, to CXCR2 induces the production of proinflammatory mediators, or induces the expression of a molecule that stimulates mediator production. In this regard, IL-8 has been shown to induce the production of LTB 4 and LTC 4 by neutrophils and IL-3-treated basophils, respectively (56,57). In addition, IL-8 has been reported to enhance the expression of cyclooxygenase-2, which catalyzes the formation of PGs such as PGE 2 , by LPS-stimulated neutrophils (58), and to act in an autocrine fashion, inducing monocyte IL-8 production (59,60).…”

Section: Discussionmentioning

confidence: 99%

A Potent and Selective Nonpeptide Antagonist of CXCR2 Inhibits Acute and Chronic Models of Arthritis in the Rabbit

Podolin

Bolognese

Foley

et al. 2002

The Journal of Immunology

146

112

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Much evidence implicates IL-8 as a major mediator of inflammation and joint destruction in rheumatoid arthritis. The effects of IL-8 and its related ligands are mediated via two receptors, CXCR1 and CXCR2. In the present study, we demonstrate that a potent and selective nonpeptide antagonist of human CXCR2 potently inhibits 125I-labeled human IL-8 binding to, and human IL-8-induced calcium mobilization mediated by, rabbit CXCR2 (IC50 = 40.5 and 7.7 nM, respectively), but not rabbit CXCR1 (IC50 = >1000 and 2200 nM, respectively). These data suggest that the rabbit is an appropriate species in which to examine the anti-inflammatory effects of a human CXCR2-selective antagonist. In two acute models of arthritis in the rabbit induced by knee joint injection of human IL-8 or LPS, and a chronic Ag (OVA)-induced arthritis model, administration of the antagonist at 25 mg/kg by mouth twice a day significantly reduced synovial fluid neutrophils, monocytes, and lymphocytes. In addition, in the more robust LPS- and OVA-induced arthritis models, which were characterized by increased levels of proinflammatory mediators in the synovial fluid, TNF-α, IL-8, PGE2, leukotriene B4, and leukotriene C4 levels were significantly reduced, as was erythrocyte sedimentation rate, possibly as a result of the observed decreases in serum TNF-α and IL-8 levels. In vitro, the antagonist potently inhibited human IL-8-induced chemotaxis of rabbit neutrophils (IC50 = 0.75 nM), suggesting that inhibition of leukocyte migration into the knee joint is a likely mechanism by which the CXCR2 antagonist modulates disease.

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“…Meanwhile, some studies showed that H pylori infection released mediators and chemokines including interleukin (IL)-8, inducible nitric oxide synthase, and COX-2 in considerable levels; among these mediators, IL-8 could stimulate lipid metabolites through modulating LOX activities [15][16][17][18][19]. Furthermore, H pylori-provoked cytokine-mediated inflammatory responses can be neutralized by blocking 5-LOX that metabolized arachidonic acid (AA) into 5(S)-HETE, a precursor metabolite of leukotrienes B 4 (LTB 4 ), suggesting that LOX pathway as much as COX induction could be principally engaged in pathogenic mechanism of H pylori infection.…”

Section: Abstract Helicobacter Pylori Red Ginseng 5(s)-hete 5-lmentioning

confidence: 99%

Inhibitory Activities and Attenuated Expressions of 5-LOX with Red Ginseng in Helicobacter pylori-Infected Gastric Epithelial Cells

et al. 2007

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Our recent studies documented that red ginseng extract (RGE, isolates from steamed and dried Panax ginseng, C.A. Meyer) can inhibit Helicobacter pylori-induced mitogen-activated protein kinase (MAPK) signaling with repressing either nuclear factor (NF)-κB-DNA binding activity or releases of IL-8 and COX-2 in gastric epithelial cells (Dig Dis Sci 50:1218-1227, 2005. We extended the experiment to prove whether RGE influences 5-lipoxygenase (5-LOX) pathway, thereby suppressing the biosynthesis of 5(S)-HETE. The 5-LOX enzyme activities were measured by thin layer chromatography using 14 C-labeled arachidonic acid (AA) and quantified by reverse phase-high performance liquid chromatography in human gastric adenocarcinoma (AGS) cells cocultured with H pylori (ATCC 43504 strain) with or without pretreatment of RGE. Western blotting analyses for MAPK signaling and 5-LOX, reverse transcriptase polymerase chain reaction for interleukin-8, and electrophoretic mobility shift assay for NF-κB-DNA binding were done, respectively. H pylori infection increased exclusively 5-LOX enzyme activity and RGE inhibited H pylori-stimulated 5-LOX activity, resulting in suppression of 5(S)-HETE generations from AA. RGE inactivated c-jun phosphorylation and repressed redox-sensitive transcriptional activation, led to reduced expression of IL-8 and 5-LOX mRNA in gastric mucosal cells, of which action was

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The monocyte-derived neutrophil activating peptide (NAP/interleukin 8) stimulates human neutrophil arachidonate-5-lipoxygenase, but not the release of cellular arachidonate.

Cited by 162 publications

References 40 publications

Pulmonary Expression of Tumor Necrosis Factor Alpha, Interleukin-1 Beta, and Interleukin-8 in the Acute Phase of Bovine Pneumonic Pasteurellosis

Pulmonary Expression of Tumor Necrosis Factor Alpha, Interleukin-1 Beta, and Interleukin-8 in the Acute Phase of Bovine Pneumonic Pasteurellosis

A Potent and Selective Nonpeptide Antagonist of CXCR2 Inhibits Acute and Chronic Models of Arthritis in the Rabbit

Inhibitory Activities and Attenuated Expressions of 5-LOX with Red Ginseng in Helicobacter pylori-Infected Gastric Epithelial Cells

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