β2-Adrenergic activation enhances interleukin-8 production by human monocytes

Kavelaars, Annemieke; Pol, Marion van de; Zijlstra, Jitske; Heijnen, Cobi J.

doi:10.1016/s0165-5728(97)00076-3

Cited by 112 publications

(61 citation statements)

References 23 publications

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“…This effect was antagonized, in females, by SB225002, a selective CXCR2 antagonist, and by a CXCR2 antibody, which has been shown to markedly inhibit IL-8-induced neutrophil migration in murine models of inflammation (Garcia-Ramallo et al, 2002). However, while b 2 -adrenergic receptor agonists can increase IL-8 production (Linden, 1996;Kavelaars et al, 1997;Prause et al, 2003), this did not appear to be the mechanism of isoprenaline-induced chemotaxis in our study. Rather, our data suggest the possibility that b 2 -adrenergic receptor activation induced the release of other cytokines that are ligands for the CXCR2 receptor, such as CXCL1 gene products (e.g.…”

Section: De Coupade Et Alcontrasting

confidence: 60%

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β₂‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

Coupade¹,

Gear²,

Dazin

et al. 2004

British J Pharmacology

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1 While the mechanisms underlying the marked sexual dimorphism in inflammatory diseases are not well understood, the sexually dimorphic sympathoadrenal axis profoundly affects the inflammatory response. We tested whether adrenergic receptor-mediated activation of human neutrophil function is sexually dimorphic, since neutrophils provide the first line of defense in the inflammatory response. 2 There was a marked sexual dimorphism in b 2 -adrenergic receptor binding, using the specific b 2 -adrenergic receptor ligand, [ 3 H]-dihydroalprenolol, with almost three times more binding sites on neutrophils from females (20,87872470) compared to males (733173179). 3 There was also a marked sexual dimorphism in the effects of isoprenaline, a b-adrenergic receptor agonist, which increased nondirected locomotion (chemokinesis) in neutrophils obtained from females, while having no effect on neutrophils from males. 4 Isoprenaline stimulated the release of a chemotactic factor from neutrophils obtained from females, but not from males. This chemotactic factor acts on the G protein-coupled CXC chemokine receptor 2 (CXCR2) chemokine receptor, since an anti-CXCR2 antibody and the selective nonpeptide CXCR2 antagonist SB225002, inhibited chemotaxis produced by this factor. While interleukin-(IL-) 8 is a principal CXCR2 ligand, isoprenaline did not produce an increase in IL-8 release from neutrophils. 5 IL-8-induced chemotaxis was inhibited in a sexually dimorphic manner by isoprenaline, which also stimulated release of a mediator from neutrophils that induced chemotaxis, that was inhibited by anti-CXCR2 antibodies. 6 These findings indicate an important role for adrenergic receptors in the modulation of neutrophil trafficking, which could contribute to sex-differences in the inflammatory response.

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Section: De Coupade Et Alcontrasting

confidence: 60%

“…Since b 2 -adrenergic receptor agonists are known to stimulate IL-8 release (Linden, 1996;Kavelaars et al, 1997), we investigated whether the released factor could be IL-8. Neutralizing antibody for CXCR2 receptors (cytokine receptors for IL-8, present on neutrophils) was added to the upper chamber along with the unstimulated cells.…”

Section: De Coupade Et Almentioning

confidence: 99%

β₂‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

Coupade¹,

Gear²,

Dazin

et al. 2004

British J Pharmacology

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“…In this regard, ␤ 2 -adrenergic agonists (␤ 2 -AR), which increase intracellular cAMP levels, were shown to induce IL-8 secretion in monocytes and bronchial epithelial cells (26,27). This fact is particularly important, because the use of ␤ 2 -AR agonists as bronchodilators can exacerbate asthma and should be used in conjunction with anti-inflammatory steroids (28).…”

Section: Discussionmentioning

confidence: 99%

Identification of a family of cAMP response element-binding protein coactivators by genome-scale functional analysis in mammalian cells

Iourgenko

Zhang

Mickanin

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

351

306

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This report describes an unbiased method for systematically determining gene function in mammalian cells. A total of 20,704 predicted human full-length cDNAs were tested for induction of the IL-8 promoter. A number of genes, including those for cytokines, receptors, adapters, kinases, and transcription factors, were identified that induced the IL-8 promoter through known regulatory sites. Proteins that acted through a cooperative interaction between an AP-1 and an unrecognized cAMP response element (CRE)-like site were also identified. A protein, termed transducer of regulated cAMP response element-binding protein (CREB) (TORC1), was identified that activated expression through the variant CRE and consensus CRE sites. TORC1 potently induced known CREB1 target genes, bound CREB1, and activated expression through a potent transcription activation domain. A functional Drosophila TORC gene was also identified. Thus, TORCs represent a family of highly conserved CREB coactivators that may control the potency and specificity of CRE-mediated responses.IL-8 ͉ genomics ͉ high-throughput screening ͉ transducer of regulated cAMP response element-binding protein

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“…Furthermore, the obvious discrepancy that TNF- § formation on the one hand is blunted by increasing cAMP but on the other hand is required for G-CSF formation has not yet been addressed. Based on our findings, G-CSF can be added to a list of cytokines like IL-6, IL-8 and IL-10, which share the same properties concerning its modulation by cAMP [49][50][51][52][53].…”

Section: Discussionmentioning

confidence: 99%

Cyclic AMP increases endogenous granulocyte colony‐stimulating factor formation in monocytes and THP‐1 macrophages despite attenuated TNF‐α formation

et al. 2003

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The cytokine granulocyte colony-stimulating factor (G-CSF) is in broad clinical use to treat neutropenia, and trials on its use in immunosuppressed conditions and infections are ongoing. To apply G-CSF effectively, it is crucial to understand the regulation and distribution of its endogenous formation. Since G-CSF release is mediated, at least in part, by TNF- § formation, we investigated whether drugs suppressing TNF- § also impair G-CSF production. Surprisingly, G-CSF formation was enhanced in lipopolysaccharide (LPS)-stimulated blood from a pentoxifylline-treated patient. In the presence of dibutyryl-cAMP, forskolin, tolafentrine or 3-isobutyl-1-methylxanthine, LPS-induced G-CSF formation was enhanced in THP-1 cells, primary monocytes and whole blood. Correspondingly, rp-8-bromo-cAMP suppressed LPS-induced G-CSF release. Addition of prostaglandin E 2 enhanced and indomethacin suppressed G-CSF formation. Reporter gene studies showed that dibutyryl-cAMP enhanced LPS-induced G-CSF promoter activity, indicating a transcriptional up-regulation. Furthermore, disruption of a newly identified putative cAMP-responsive element (CRE) in the G-CSF promoter demonstrated the regulatory role for G-CSF gene transcription. In conclusion, endogenous G-CSF formation critically depends on both TNF- § and cyclooxygenase products, exerting effects via cAMP and the CRE in the G-CSF promoter. This might have bearing for drug side effects, putative G-CSF mimetics and our understanding of G-CSF immunobiology.

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β2-Adrenergic activation enhances interleukin-8 production by human monocytes

Cited by 112 publications

References 23 publications

β₂‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

β₂‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

Identification of a family of cAMP response element-binding protein coactivators by genome-scale functional analysis in mammalian cells

Cyclic AMP increases endogenous granulocyte colony‐stimulating factor formation in monocytes and THP‐1 macrophages despite attenuated TNF‐α formation

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β2-Adrenergic activation enhances interleukin-8 production by human monocytes

Cited by 112 publications

References 23 publications

β2‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

β2‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

Identification of a family of cAMP response element-binding protein coactivators by genome-scale functional analysis in mammalian cells

Cyclic AMP increases endogenous granulocyte colony‐stimulating factor formation in monocytes and THP‐1 macrophages despite attenuated TNF‐α formation

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β₂‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

β₂‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic