Glucocorticoids induce basophil apoptosis

Yoshimura, Chitose; Miyamasu, Misato; Nagase, Hiroyuki; Iikura, Motoyasu; Yamaguchi, Masao; Kawanami, Oichi; Morita, Yutaka; Iwata, Tadahisa; Yamamoto, Kazuhiko; Hirai, Koichi

doi:10.1067/mai.2001.116575

Cited by 63 publications

(48 citation statements)

References 23 publications

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“…As noted, GCs have profound negative effects on the numbers of circulating leukocytes and can induce apoptosis (Yoshimura et al 2001). However, a closer look reveals that neutrophil proliferation and survival are enhanced by GCs (Cox 1995;Liles et al 1995) and that the largescale depletion of other leukocytes may actually reflect extravasation to a site of injury, rather than cell death (Dhabhar et al 1996;Dhabhar and McEwen 1997;Viswanathan and Dhabhar 2005).…”

Section: The Pro-inflammatory Effects Of Gcs Outside the Nervous Systemmentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

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In recent years the classic view that glucocorticoids, the adrenal steroids secreted during stress, are universally anti-inflammatory has been challenged at a variety of levels. It was first observed that under some circumstances, acute GC exposure could have pro-inflammatory effects on the peripheral immune response. More recently, chronic exposure to GCs has been found to have pro-inflammatory effects on the specialized immune response to injury in the central nervous system. Here we review the evidence that in some cases, glucocorticoids can increase pro-inflammatory cell migration, cytokine production, and even transcription factor activity in the brain. We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings.

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Section: The Pro-inflammatory Effects Of Gcs Outside the Nervous Systemmentioning

confidence: 99%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

View full text Add to dashboard Cite

show abstract

“…Measurement of apoptotic and live cells was performed using an MEBCYTO apoptosis kit (MBL) and flow cytometer as previously described (26). In brief, early apoptotic cells were identified by their ability to bind annexin V and exclude propidium iodide (PI).…”

Section: Survival Assaymentioning

confidence: 99%

An IL-1 Cytokine Member, IL-33, Induces Human Basophil Activation via Its ST2 Receptor

Suzukawa

Iikura

Koketsu

et al. 2008

The Journal of Immunology

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282

231

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Basophils are thought to play pivotal roles in allergic inflammation through rapid release of chemical mediators in addition to sustained production of Th2 cytokines, including IL-4. A newly identified cytokine, IL-33, has been recognized as one of the key cytokines enhancing Th2-balanced immune regulation through its receptor, ST2. The present study was conducted to elucidate whether IL-33 acts directly on, and affects the functions of, human basophils. Real-time PCR analysis showed that basophils express transcripts for ST2. The expression levels were significantly higher compared with eosinophils and neutrophils, and treatment with IL-33 significantly up-regulated basophil ST2 mRNA expression. Expressions of IL-4 and IL-13 mRNA were also up-regulated by IL-33, and there was also enhanced secretion of IL-4 protein. IL-33 increased the surface levels of basophil CD11b expression and enhanced basophil adhesiveness. Although IL-33 failed to directly induce degranulation or attract basophils, it exerted priming effects on basophils. It enhanced degranulation in response to IgE-crosslinking stimulus and also enhanced basophil migration toward eotaxin without changing surface CCR3. Also, IL-33 synergistically enhanced IL-4 production and CD11b expression by IL-3-stimulated basophils. Neutralization using Ab specific for ST2 significantly diminished the enhancing effects of IL-33 on both basophil CD11b expression and migration toward eotaxin, indicating that IL-33 signals via ST2 expressed on basophils. This study revealed that IL-33 potently regulates migration and activation of human basophils. IL-33 may be a key cytokine in the pathogenesis of Th2-dominant inflammation by acting not only on lymphocytes but also on effector cells such as basophils.

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“…Differential analysis of apoptotic and live cells was performed using a MEBCYTO apoptosis kit (MBL) and flow cytometry as previously described. 19 Early apoptotic cells were quantitatively determined by their ability to bind annexin V and exclude propidium iodide (PI). Cells stained with PI were considered to be necrotic cells.…”

Section: Survival Assaymentioning

confidence: 99%

Interleukin-33 enhances adhesion, CD11b expression and survival in human eosinophils

Suzukawa

Koketsu

Iikura

et al. 2008

Laboratory Investigation

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186

154

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Eosinophils are important effector cells in allergic diseases, but the mechanisms regulating their biological functions remain obscure. Interleukin-33 (IL-33) is a recently identified cytokine of the IL-1 family, and it reportedly accelerates the production of Th2-associated cytokines and promotes tissue inflammation. However, the action of IL-33 on effector cells such as eosinophils has remained unclear. In this study, we investigated the effects of IL-33 on eosinophil activation, assessed in terms of the cells' adhesiveness, expression of CD11b and apoptosis. Adhesiveness was quantified by measuring eosinophil peroxidase content of adherent eosinophils, and expression of CD11b was measured by flow cytometry. Apoptosis was determined by flow cytometry based on the ability of cells to bind annexin V. Real-time PCR analysis showed that eosinophils expressed mRNA for ST2, a putative receptor for IL-33. IL-33 at 1-100 ng/ml enhanced the adhesiveness and CD11b expression of eosinophils even more potently than IL-5. IL-33 maintained the viability of eosinophils. Treatment with neutralizing antibodies to ST2 eliminated the effects of IL-33 on eosinophil CD11b expression and cell survival. However, IL-33 did not elicit degranulation or leukotriene C4 synthesis in eosinophils. These findings indicate that IL-33 potently induces eosinophil adhesion and CD11b expression and enhances eosinophil survival. The IL-33-ST2 pathway might be an important regulator of eosinophil biology in the pathogenesis of Th2-biased allergic diseases.

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Glucocorticoids induce basophil apoptosis

Cited by 63 publications

References 23 publications

An inflammatory review of glucocorticoid actions in the CNS

An inflammatory review of glucocorticoid actions in the CNS

An IL-1 Cytokine Member, IL-33, Induces Human Basophil Activation via Its ST2 Receptor

Interleukin-33 enhances adhesion, CD11b expression and survival in human eosinophils

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