Subacute Treatment of Rats with Dexamethasone Reduces ICAM-1 Levels on Circulating Monocytes

Tailor, Anitaben; Das, Anuk; Getting, Stephen J.; Flower, Roderick J.; Perretti, Mauro

doi:10.1006/bbrc.1997.6168

Cited by 27 publications

(20 citation statements)

References 12 publications

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“…Species-dependent differences may help explain why murine mast cell degranulation was found to be sensitive to glucocorticoid treatment [90]. Moreover, the timing and the dose of the applied steroid critically determine the anti-inflammatory effects, for example it has been shown that acute treatment with high doses of glucocorticoids is less effective than chronic low dose treatment [91]. Acute glucocorticoid treatment does not reduce the Vol.…”

Section: Glucocorticoids Attenuate Mast Cell-dependent Recruitment Ofmentioning

confidence: 99%

Neutrophil recruitment in mast cell-dependent inflammation: inhibitory mechanisms of glucocorticoids

Schramm

Thorlacius

2004

Inflamm. res.

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Mast cells are strategically localized along the microvasculature in tissues in close contact with the external environment, such as the skin, lung and intestines. By releasing a multi-faceted spectrum of proinflammatory mediators, such as cytokines and chemokines, mast cells have the capacity to coordinate trafficking of leukocytes. Mast cells play a pathophysiological role in numerous inflammatory diseases as diverse as hypersensitivity reactions, ischemia/reperfusion injury and rheumatoid arthritis. On the other hand, mast cells act also as tissue sentinels and are critically involved in the host defensive response against microbial infection by stimulating neutrophil recruitment. Glucocorticoids are powerful agents frequently used in mast cell-dependent diseases, although the anti-inflammatory mechanisms of these compounds are not completely understood at present. In order to circumvent steroid-associated side-effects and develop more specific therapeutics, numerous studies have examined the mechanisms underlying glucocorticoid inhibition of mast cell-dependent neutrophil recruitment. Based on recent findings, it may be suggested that glucocorticoids selectively inhibit the expression and function of certain adhesion molecules and chemokines. This review summarizes current insights into the underlying mechanisms of mast cell-regulated tissue accumulation of neutrophils and the inhibitory effects of glucocorticoids.

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Section: Glucocorticoids Attenuate Mast Cell-dependent Recruitment Ofmentioning

confidence: 99%

Neutrophil recruitment in mast cell-dependent inflammation: inhibitory mechanisms of glucocorticoids

Schramm

Thorlacius

2004

Inflamm. res.

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“…Interleukin 10 (IL-10) is an antiinflammatory cytokine that has a number of effects in common with GCs, particularly those affecting macrophage functions. Both GCs [1][2][3][4][5][6][7][8][9][10][11][12][13] and IL-10 (reviewed in Stordeur and Goldman 14 ) inhibit antigen processing, the expression of HLA, CD80, and CD86, and the synthesis of nitric oxide, cyclo-oxygenase 2, adhesion molecules, cytokines, and chemokines. The intracellular events induced by the binding of GCs and IL-10 to their respective receptors are not fully understood, but they also share certain characteristics.…”

Section: Introductionmentioning

confidence: 99%

Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10

Berrebi

Bruscoli

Cohen

et al. 2003

Blood

261

281

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Glucocorticoids and interleukin 10 (IL-10) prevent macrophage activation. In murine lymphocytes, glucocorticoids induce expression of glucocorticoid-induced leucine zipper (GILZ), which prevents the nuclear factor B (NF-B)-mediated activation of transcription. We investigated whether GILZ could account for the deactivation of macrophages by glucocorticoids and IL-10. We found that GILZ was constitutively produced by macrophages in nonlymphoid tissues of humans and mice. Glucocorticoids and IL-10 stimulated the production of GILZ by macrophages both in vitro and in vivo. Transfection of the macrophagelike cell line THP-1 with the GILZ gene inhibited the expression of CD80 and CD86 and the production of the proinflammatory chemokines regulated on activation normal T-cell expressed and secreted (CCL5) and macrophage inflammatory protein 1␣ (CCL3). It also prevented toll-like receptor 2 production induced by lipopolysaccharide, interferon␥, or an anti-CD40 mAb, as well as NF-B function. In THP-1 cells treated with glucocorticoids or IL-10, GILZ was associated with the p65 subunit of NF-B. Activated macrophages in the granulomas of patients with Crohn disease or tuberculosis do not produce GILZ. In contrast, GILZ production persists in tumorinfiltrating macrophages in Burkitt lymphomas. Therefore, GILZ appears to play a key role in the anti-inflammatory and immunosuppressive effects of glucocorticoids and IL-10. Glucocorticoid treatment stimulates GILZ production, reproducing an effect of IL-10, a natural anti-inflammatory agent. The development of delayedtype hypersensitivity reactions is associated with the down-regulation of GILZ gene expression within lesions. In contrast, the persistence of GILZ gene expression in macrophages infiltrating Burkitt lymphomas may contribute to the failure of the immune system to reject the tumor. IntroductionGlucocorticoids (GCs) are potent anti-inflammatory and immunosuppressive drugs. Their therapeutic effects are largely due to their ability to inhibit many functions of macrophages and of other antigen-presenting cells. Interleukin 10 (IL-10) is an antiinflammatory cytokine that has a number of effects in common with GCs, particularly those affecting macrophage functions. Both GCs 1-13 and IL-10 (reviewed in Stordeur and Goldman 14 ) inhibit antigen processing, the expression of HLA, CD80, and CD86, and the synthesis of nitric oxide, cyclo-oxygenase 2, adhesion molecules, cytokines, and chemokines. The intracellular events induced by the binding of GCs and IL-10 to their respective receptors are not fully understood, but they also share certain characteristics. In particular, both GCs and IL-10 interfere with the function of the transcriptional activators AP-1 and NF-B (reviewed in Stordeur and Goldman, 14 Karin, 15 and Barnes and Karin 16 ). Pathogenassociated molecular patterns (PAMPs) of bacterial components activate macrophages by binding to the toll-like receptors (TLRs), which trigger the nuclear factor B (NF-B) pathway and stimulate the production of inflammatory protein...

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“…ICAM-1 has been previously demonstrated to be expressed on circulating unstimulated rodent monocytes with negligible amounts expressed on neutrophils. 30 We therefore postulated that careful administration of low doses of anti-ICAM-1 to the primary antibody cocktail would increase the purity of the neutrophil isolate without severely compromising yield. We found this to be a highly successful approach because addition of anti-ICAM-1 to the antibody cocktail increased the purity of the isolated neutrophil populations from 85 to Ͼ95%.…”

Section: Discussionmentioning

confidence: 99%

“…A leukocyte differential count for the strain of donor mouse used was also performed. Antibodies to cell surface markers were selected based on published data 29,30 to specifically label non-neutrophil cell types. In murine peripheral blood these are lymphocytes and monocytes.…”

Section: Immunomagnetic Cell Separationmentioning

confidence: 99%

A Novel Method for Isolation of Neutrophils from Murine Blood Using Negative Immunomagnetic Separation

Cotter

Norman

Hellewell

et al. 2001

The American Journal of Pathology

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Inappropriate neutrophil activation has been implicated in the pathology of several clinically important inflammatory conditions. Although murine models are extensively used in the investigation of such pathological processes, a reliable method by which viable, quiescent neutrophils can be isolated from murine blood has not been developed. Here we describe a novel method based on negative immunomagnetic separation, which yields highly pure populations of murine neutrophils. Blood is incubated with a cocktail of antibodies against specific cell markers on unwanted cells, and then with secondary antibody-coated magnetic beads. After running the preparation through a column within a magnetic field, labeled cells are retained, and a neutrophil-rich effluent is collected. This method yields a >95% pure suspension of >97% viable neutrophils, recovering ϳ70% of neutrophils from whole blood. Flow cytometric analysis shows little difference in surface Lselectin and CD18 expression on isolated neutrophils compared with neutrophils in whole blood, indicating that neutrophils are minimally activated by the isolation process. Stimulation with phorbol 12-myristate 13-acetate (PMA) reduced L-selectin and increased CD18 expression. Isolated neutrophils migrate under agarose in response to fMLP, and fluorescently labeled neutrophils transfused into recipient mice interact with postcapillary venules in a manner comparable to endogenous leukocytes. These findings show that neutrophils isolated using this method can be used for inflammatory studies in vitro and in vivo.

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Subacute Treatment of Rats with Dexamethasone Reduces ICAM-1 Levels on Circulating Monocytes

Cited by 27 publications

References 12 publications

Neutrophil recruitment in mast cell-dependent inflammation: inhibitory mechanisms of glucocorticoids

Neutrophil recruitment in mast cell-dependent inflammation: inhibitory mechanisms of glucocorticoids

Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10

A Novel Method for Isolation of Neutrophils from Murine Blood Using Negative Immunomagnetic Separation

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