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IgE Modulates Neutrophil Survival in Asthma: Role of Mitochondrial Pathway¹

Arash Shoja Saffar^*,, Martin P. Alphonse^*, Lianyu Shan^*, Kent T. HayGlass^*,, F. Estelle R. Simons^, and Abdelilah Soussi Gounni^2,*,

^* Department of Immunology and Department of Pediatrics and Child Health, and Canadian Institutes of Health Research National Training Program in Allergy and Asthma Research, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

The high-affinity IgE receptor (FcRI) has recently been reported to be expressed by neutrophils in atopic asthmatic individuals, leading to speculations that IgE could influence biological functions of these cells. In this study, we demonstrate that monomeric human IgE delayed spontaneous apoptosis of primary human neutrophils from atopic asthmatics in vitro. This effect was not dependent on FcRI cross-linking or autocrine release of soluble mediators; however, it was associated with increased expression of the antiapoptotic myeloid cell leukemia-1 protein, retention of the proapoptotic molecule Bax in the cytoplasm, decreased release of Smac from mitochondria, and reduced caspase-3 activity. Taken together, our results indicate that in vitro IgE can delay programmed cell death of neutrophils from allergic asthmatics and this may possibly contribute to neutrophilic inflammation in atopic asthma.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This study was supported by research grants from the Canadian Institutes of Health Research. A.S.G. is supported by a Canadian Institutes of Health Research New Investigator Scholarship. A.S.S. is supported by studentships from the Canadian Institutes of Health Research-sponsored National Training Program in Allergy and Asthma, Manitoba Health Research Council and the Health Sciences Centre Foundation Olenick Award in Immunology Research.

² Address correspondence and reprint requests to Dr. Abdelilah Soussi Gounni, Department of Immunology, University of Manitoba, Faculty of Medicine, 606 BMSB, 730 William Avenue, Winnipeg, Manitoba, R3E 0W3 Canada. E-mail address: gounni{at}cc.umanitoba.ca

³ Abbreviations used in this paper: AA, atopic asthmatic; PI, propidium iodide; Mcl-1, myeloid cell leukemia-1; Smac, second mitochondrial activator of caspases.

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