Divergent effects of tumour necrosis factor‐alpha on apoptosis of human neutrophils

Berg, Johanna; Weyer, S.; Weening, Jan J.; Roos, Dirk; Kuijpers, TW

doi:10.1111/rp10.1113-jphysiol.2006.109561

Cited by 43 publications

(67 citation statements)

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“…When evaluating the role of this cytokine on the neutrophil life span one should be aware that this cytokine can exert either an antior a pro-apoptotic effect, depending upon the concentration used and the time of exposure [28,41]. Interestingly, the anti-apoptotic effect of TNF-α is partly ascribed to the stimulation of a survival pathway involving activation of NF-κB [22].…”

Section: Discussionmentioning

confidence: 99%

NF-?B inhibition accelerates apoptosis of bovine neutrophils

2005

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-Apoptosis is one of the major events that contribute to the regulation of the immune system. For human neutrophils, evidence has been produced that the transcription factor NF-κB is critical in influencing the ultimate outcome of a cell's fate. However, such research has not yet been performed on bovine neutrophils. This urged us to examine the possible involvement of NF-κB in apoptosis of these cells. At first, we investigated whether p65 and p50, the most important members of the NF-κB family, are expressed in isolated blood neutrophils. The presence of both members was demonstrated on the RNA and protein level. Then the effect on bovine neutrophil apoptosis of gliotoxin, a potent and specific inhibitor of NF-κB, was examined. The rate of constitutive apoptosis was found to be greatly accelerated by inhibition of NF-κB. Furthermore, gliotoxin dramatically augmented the limited pro-apoptotic effect of TNF-α, an important inflammatory mediator. The results were obtained in six cows by annexin-V-FITC staining of externalized phosphatidylserine and subsequent flow cytometric analysis. Additional measurement of caspase-3/7 activity and evaluation of morphological criteria confirmed the outcome of this experiment. Finally, NF-κB activity was assessed under these conditions. The activity of p50 was found to be minimally affected by gliotoxin, while significantly lower active p65 values were observed. Still, the highest percentage of apoptosis, which was caused by incubation with both gliotoxin and TNF-α, did not correspond to the lowest activity of p65. We conclude that NF-κB p65 promotes the survival of bovine neutrophils by delaying the initiation of apoptosis.bovine neutrophil / NF-κB / apoptosis

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Section: Discussionmentioning

confidence: 99%

NF-?B inhibition accelerates apoptosis of bovine neutrophils

2005

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“…TNF-␣ is a unique proinflammatory cytokine whose signaling is linked to both antiapoptotic and proapoptotic pathways (3,10,12,23,39,42,54). The cellular response to TNF-␣ is dependent on cytokine levels, length of exposure, and input from other signaling pathways (i.e., engagement of integrins).…”

Section: Discussionmentioning

confidence: 99%

“…TNF-␣ is a unique proinflammatory cytokine whose signaling pathways are linked to both antiapoptotic and proapoptotic responses in neutrophils (3,10,12,23,39,42,54). Neutrophils possess two TNF-␣ receptors, a 55-60 kDa (p60TNFR) and a 75-80 kDa (p80TNFR), and both antiapoptotic and proapoptotic signaling pathways are regulated principally by the p60TNFR (4,33,49).…”

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confidence: 99%

“…The increased survival of neutrophils may contribute to the pathophysiology of these inflammatory diseases through excessive release of toxic mediators, resulting in host tissue damage and organ dysfunction. Tumor necrosis factor (TNF)-␣ and other proinflammatory cytokines have been implicated as endogenous mediators responsible for the modulation of neutrophil apoptosis during inflammation (10,12,14,18,22,23,27,31,34,37,39,42,54).…”

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confidence: 99%

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A role for PKC-δ and PI 3-kinase in TNF-α-mediated antiapoptotic signaling in the human neutrophil

Kilpatrick

Lee

Haines

et al. 2002

American Journal of Physiology-Cell Physiology

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The proinflammatory cytokine tumor necrosis factor (TNF)-α has been implicated in the attenuation of neutrophil spontaneous apoptosis during sepsis. Antiapoptotic signaling is principally mediated through the p60TNF receptor (p60TNFR). In neutrophils, TNF-α is an incomplete secretagogue and requires input from a ligated integrin(s) for neutrophil activation. In adherent neutrophils, TNF-α triggers association of both protein kinase C (PKC)-δ and phosphatidylinositol (PI) 3-kinase with the p60TNFR. In this study, a role for PKC-δ and PI 3-kinase in TNF-α-mediated antiapoptotic signaling was examined. TNF-α inhibited spontaneous apoptosis in fibronectin-adherent neutrophils, and this antiapoptotic signaling was blocked by the PKC-δ inhibitor rottlerin, but not by an inhibitor of Ca2+-dependent PKC isotypes, Go-6976. Inhibition of PI 3-kinase by LY-294002 also inhibited TNF-α-mediated antiapoptotic signaling. Cycloheximide blocked TNF-α-mediated antiapoptotic signaling, suggesting protein synthesis is required. Inhibition of either PKC-δ or PI 3-kinase attenuated TNF-α-mediated activation of the antiapoptotic transcription factor NFκB. Thus both PKC-δ and PI 3-kinase have essential roles in TNF-α-mediated antiapoptotic signaling in adherent neutrophils.

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“…TNF-α is one of the most important orchestrators of inflammation. However, when evaluating the effect of this cytokine on the lifespan of PMN one should be aware that it can exert either anti-or pro-apoptotic effects depending on the concentration, time of exposure and cell type [24,34,38]. The evaluation of the effect of pro-apoptotic doses of TNF-α on the lifespan of bovine PMN resulted in a slight, albeit non significant stimulation of apoptosis [25].…”

Section: Discussionmentioning

confidence: 99%

Influence of sex steroids on the viability and CD11b, CD18 and CD47 expression of blood neutrophils from dairy cows in the last month of gestation

et al. 2006

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-In the period around parturition, cows experience an increased susceptibility for the development of Escherichia coli mastitis. This increased susceptibility has been correlated with a decreased functionality of neutrophils. In the current study, it is suggested that the decreased neutrophil functionality may be induced by the extensive alterations in sex steroid levels occurring around parturition. It was first hypothesized that 17β-estradiol and progesterone influence the viability, apoptosis and necrosis of blood neutrophils from cows in their last month of gestation. Subsequently, it was hypothesized that 17β-estradiol modulates the expression of CD11b, CD18 or CD47 thereby explaining its influence on the migration of bovine neutrophils. Neither 17β-estradiol nor progesterone significantly influenced viability, apoptosis or necrosis in spontaneous apoptosis conditions. However, when apoptosis was induced with TNF-α and gliotoxin, progesterone exerted a survival effect (P < 0.05). In addition, 17β-estradiol treatment of bovine blood neutrophils significantly decreased the expression of CD47 (P < 0.05) but not of CD11b or CD18. It can be concluded that 17β-estradiol and progesterone do not affect spontaneous apoptosis of bovine blood neutrophils while a survival effect was observed for progesterone on induced neutrophils apoptosis. Moreover, our results concerning the influence of 17β-estradiol on the CD11b, CD18 and CD47 expression extend previous demonstrations of the suppressive effect of 17β-estradiol on neutrophils migration and indicate that the altered expression of CD47 may contribute to this phenomenon. sex steroid / β 2 -integrin / CD47 / viability / polymorphonuclear neutrophil leukocyte

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Divergent effects of tumour necrosis factor‐alpha on apoptosis of human neutrophils

Cited by 43 publications

References 0 publications

NF-?B inhibition accelerates apoptosis of bovine neutrophils

NF-?B inhibition accelerates apoptosis of bovine neutrophils

A role for PKC-δ and PI 3-kinase in TNF-α-mediated antiapoptotic signaling in the human neutrophil

Influence of sex steroids on the viability and CD11b, CD18 and CD47 expression of blood neutrophils from dairy cows in the last month of gestation

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