CD40 engagement enhances eosinophil survival through induction of cellular inhibitor of apoptosis protein 2 expression: Possible involvement in allergic inflammation

Bureau, Fabrice; Seumois, Grégory; Jaspar, Fabrice; Vanderplasschen, Alain; Detry, Bruno; Pastoret, Paul-Pierre; Louis, Renaud; Lekeux, Pierre

doi:10.1067/mai.2002.126781

Cited by 37 publications

(27 citation statements)

References 32 publications

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“…This cell cycle configuration is typical of cells that are undergoing active proliferation. These data are compatible with those of previous reports on the effects of CD40 in other cell types (26,27,32).…”

Section: Discussionsupporting

confidence: 83%

CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death

Merendino

Bucchieri²,

Gagliardo³

et al. 2006

Am J Respir Cell Mol Biol

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CD40 and its ligand regulate pleiotropic biological responses, including cell proliferation, differentiation, and apoptosis. In many inflammatory lung diseases, tissue damage by environmental or endogenous oxidants plays a major role in disease pathogenesis. As the epithelial barrier is a major target for these oxidants, we postulated that CD40, the expression of which is increased in asthma, plays a role in the regulation of apoptosis of bronchial epithelial cells exposed to oxidants. Using 16HBE 14o؊ cells exposed to oxidant stress, we found that ligation of CD40 (induced by G28-5 monoclonal antibodies) enhanced cell survival and increased the number of cells in G2/M (interphase between DNA synthesis and mitosis) of the cell cycle. This was associated with NF-B and activator protein-1 activation and increased expression of the inhibitor of apoptosis, c-IAP1. However, oxidant stress-induced apoptosis was found to be caspase-and calpain-independent implicating CD40 ligation as a regulator of caspase-independent cell death. This was confirmed by the demonstration that CD40 ligation prevented mitochondrial release and nuclear translocation of apoptosis inducing factor. In conclusion, we demonstrate a novel role for CD40 as a regulator of epithelial cell survival against oxidant stress. Furthermore, we have identified, for the first time, an endogenous inhibitory pathway of caspase-independent cell death.

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Section: Discussionsupporting

confidence: 83%

CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death

Merendino

Bucchieri²,

Gagliardo³

et al. 2006

Am J Respir Cell Mol Biol

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“…In addition, WOOLLEY et al [5] demonstrated an increase in the sputum eosinophil AR and a decrease in sputum eosinophil numbers following corticosteroid treatment of patients with induced asthma exacerbation. Therefore, delayed eosinophil apoptosis may be an important cause of the increased tissue load of eosinophils seen in asthma [9,10]. However, a recent study by GIBSON et al [8] investigating the anti-inflammatory effects of a single high dose of inhaled budesonide reported that a subsequent decrease in the percentage sputum eosinophils following treatment was not accompanied by an increase in the proportion of apoptotic eosinophils.…”

Section: Discussionmentioning

confidence: 90%

“…However, to date there have been few studies that have utilised this technique to compare the relationship between measures of eosinophil apoptosis or survival in induced sputum with clinical and functional parameters of disease severity [5][6][7][8][9][10]. The authors hypothesised that there is a relationship between reduced eosinophil apoptosis and both a global clinical severity score and separate components of the asthma phenotype.…”

mentioning

confidence: 99%

Reduced eosinophil apoptosis in induced sputum correlates with asthma severity

et al. 2003

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This study was carried out to investigate the relationship between induced sputum eosinophil apoptosis and clinical severity score, airway obstruction and symptom scores in patients with chronic stable asthma.Altogether, 41 chronic stable asthmatic subjects of varying severity defined by Aas score and 17 control subjects underwent spirometry, symptom questionnaire and successful sputum induction. Sputum was processed and cytospins prepared for light microscopy to determine normal and apoptotic eosinophils.Mild asthmatic subjects had a significantly lower percentage sputum eosinophils and a significantly higher eosinophil apoptotic ratio (AR) than moderate or chronic severe asthmatics. Severe asthmatic subjects had a significantly greater age, duration of asthma and sputum eosinophil count?mL -1 than mild asthmatic subjects. Asthmatic subjects9 symptom scores, severity scores and age inversely correlated with AR and the percentage of sputum eosinophils. Baseline forced expiratory volume in one second inversely correlated with percentage sputum eosinophils and positively correlated with AR.The study demonstrates a relationship between reduced sputum eosinophil apoptosis and increased clinical severity of chronic stable asthma, providing additional evidence that eosinophil apoptosis may be important in the resolution of eosinophilic airway inflammation in asthma. Eur Respir J 2003; 22: 484-490.

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“…Thus, its expression is tightly regulated both at the transcriptional and translational levels. Indeed, in certain instances, cIAP2 mRNA is present in the absence of cIAP2 protein (1,30).…”

mentioning

confidence: 99%

Translation of cIAP2 mRNA Is Mediated Exclusively by a Stress-Modulated Ribosome Shunt

Sherrill

Lloyd

2008

Molecular and Cellular Biology

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During cellular stress, translation persists or increases for a number of stress-responsive proteins, including cellular inhibitor of apoptosis 2 (cIAP2). The cIAP2 transcript includes a very long (2.78-kb) 5 untranslated region (UTR) with an unusually high number of upstream AUGs (uAUGs), i.e., 64, and a stable predicted secondary structure (⌬G Х ؊620 kcal/mol) that should completely block conventional scanning-dependent translation initiation. This region did not facilitate internal ribosome entry in vitro or when RNA reporter transcripts were transfected into cells. However, several structural features within the cIAP2 5 UTR were observed to be nearly identical to those required for ribosome shunting in cauliflower mosaic virus RNA and are well conserved in cIAP2 orthologs. Selective mutation revealed that the cIAP2 mRNA mediates translation exclusively via ribosome shunting that bypasses 62 uAUGs. In addition, shunting efficiency was altered by stress and was greatly facilitated by a conserved RNA folding domain (1,470 to 1,877 nucleotides upstream) in a region not scanned by shunting ribosomes. This arrangement suggests that regulation of cIAP2 shunting may involve recruitment of RNA binding proteins to modulate the efficiency of translation initiation.

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CD40 engagement enhances eosinophil survival through induction of cellular inhibitor of apoptosis protein 2 expression: Possible involvement in allergic inflammation

Cited by 37 publications

References 32 publications

CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death

CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death

Reduced eosinophil apoptosis in induced sputum correlates with asthma severity

Translation of cIAP2 mRNA Is Mediated Exclusively by a Stress-Modulated Ribosome Shunt

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