Augmentation of Apoptosis in Bronchial Exuded Rat Eosinophils by Cyclosporin A

Kitagaki, Kunihiko; Niwa, Satoru; Hoshiko, Ken-ichiro; Nagai, Hiroichi; Hayashi, Shigehiro; Totsuka, Teruji

doi:10.1006/bbrc.1996.0715

Cited by 18 publications

(10 citation statements)

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“…To date, there is no evidence that CsA induces neutrophil apoptosis. Although some in vitro studies have shown CsA-augmented apoptosis of rat or mouse eosinophils [26,27], CsA-induced apoptosis of eosinophils was not observed in the present study (table 2). Previous observations show that CsA does not directly induce human eosinophil apoptosis in vitro [28].…”

Section: Discussioncontrasting

confidence: 87%

Cyclosporin A, apoptosis of BAL T-cells and expression of Bcl-2 inasthmatics

Sun¹,

Khan²,

Meng³

et al. 2003

European Respiratory Journal

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Section: Discussioncontrasting

confidence: 87%

Cyclosporin A, apoptosis of BAL T-cells and expression of Bcl-2 inasthmatics

Sun¹,

Khan²,

Meng³

et al. 2003

European Respiratory Journal

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“…NR = not reported glucocorticoids enhance eosinophil apoptosis in vitro, but most of the relevant data has been limited to dexamethasone and prednisolone [104,140,[144][145][146][147][148]. Recently, the effects of currently used inhaled glucocorticoids on eosinophil apoptosis were studied [120,121].…”

Section: Immunosuppressive Compoundsmentioning

confidence: 99%

Pharmacological Regulation of Human Eosinophil Apoptosis

Kankaanranta

Moilanen²,

Zhang

2005

CDTIA

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Eosinophilic inflammation of the airways is a key characteristic of asthma. The balance between eosinophil recruitment into the lung and their removal from the lungs determines the number of eosinophils in the airways. Apoptosis or programmed cell death is of importance in the removal of eosinophils from the lungs. In asthma, eosinophil apoptosis is delayed. Glucocorticoids enhance eosinophil apoptosis, whereas beta(2)-agonists may delay apoptosis in eosinophils. Detailed knowledge on the mechanisms that regulate this process gives an opportunity to develop specific asthma therapies targeting the eosinophil. This review aims to focus on the signalling leading to or preventing apoptosis in human eosinophils as well as reviews the current evidence on the regulation of eosinophil apoptosis and/or survival in allergic diseases.

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“…It could increase the number of E-selectin-expressing endothelial cells and the intensity and the duration of this expression [67]. It fails to significantly inhibit TNF-α mRNA in normal and LPS-treated mice [68], and it could induce apoptosis in some tumoral or normal cells via different pathways [69, 70, 71, 72, 73, 74]. …”

Section: Csa Limitationsmentioning

confidence: 99%

Would Cyclosporin A Be Beneficial to Mitigate Drug-Induced Toxic Epidermal Necrolysis?

Paquet¹,

Pierard²

1999

Dermatology

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Drug-induced toxic epidermal necrolysis (TEN) is a rare life-threatening disease whose mortality remains high. The treatment of the disease is badly settled. Several kinds of drugs have been tested, including systemic corticosteroids, cyclophosphamide, pentoxifylline and thalidomide, but without any clear-cut outcome. Cyclosporin A (CsA) has many inhibitory effects on the main cell populations involved in TEN (T lymphocytes, macrophages and keratinocytes). CsA could also act on tumor necrosis factor α metabolism, a cytokine which is important in TEN epidermal destruction. Moreover, apoptosis is the mechanism leading to keratinocyte death and CsA has antiapoptotic properties. CsA has already been used successfully on a limited series of TEN patients. We have reviewed the potential theoretical useful effects of CsA in TEN. We conclude that CsA could be a good candidate to reverse TEN progression.

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Augmentation of Apoptosis in Bronchial Exuded Rat Eosinophils by Cyclosporin A

Cited by 18 publications

References 0 publications

Cyclosporin A, apoptosis of BAL T-cells and expression of Bcl-2 inasthmatics

Cyclosporin A, apoptosis of BAL T-cells and expression of Bcl-2 inasthmatics

Pharmacological Regulation of Human Eosinophil Apoptosis

Would Cyclosporin A Be Beneficial to Mitigate Drug-Induced Toxic Epidermal Necrolysis?

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