Rapid acceleration of neutrophil apoptosis by tumor necrosis factor-α

Takeda, Yuji; Watanabe, Hiroshi; Yonehara, Shin; Yamashita, T; Saito, Sayaka; Sendo, Fujiro

doi:10.1093/intimm/5.6.691

Cited by 140 publications

(72 citation statements)

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“…The results of a study by Coxon et al [32] attribute a major role to CD11b/CD18, a ␤ 2 integrin, in triggering apoptosis in activated, as opposed to resting, neutrophils, thereby regulating the magnitude of neutrophil extravasation to the TG-inflamed peritoneum of mice. Neutrophils also are sensitive to apoptosis induced by TNF-␣ or IL-6 [28][29][30][31], two cytokines known to be involved in inflammatory responses [56]. Furthermore, Fas is but one member of a recently discovered family of so-called death factor receptors that also includes the TNF receptor I, DR3/WSL-1, and CAR1 [see ref.…”

Section: Discussionmentioning

confidence: 99%

“…FasL/Fas interactions might be expected to play a role in triggering the apoptosis of neutrophils at an inflammatory site. Neutrophils also possess several receptors besides Fas that could trigger their apoptosis, including receptors for the inflammatory cytokines TNF-␣ and IL-6, and for the ␤ 2 integrin CD11b/CD18 [28][29][30][31][32].…”

Section: Introductionmentioning

confidence: 99%

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Fas ligand (gld)- and Fas (lpr)-deficient mice do not show alterations in the extravasation or apoptosis of inflammatory neutrophils

Fecho

Cohen

1998

Journal of Leukocyte Biology

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Apoptosis of neutrophils plays a critical role in the resolution of acute inflammation. Neutrophils from human peripheral blood express Fas (CD95) and are sensitive to Fas ligand (FasL)/Fasmediated apoptosis. Mice carrying spontaneous mutations in the genes for fas ligand (B6/gld) or fas (B6/lpr) were used to assess the role of FasL/Fas in the kinetics and magnitude of neutrophil extravasation to the thioglycolate (TG)-inflamed peritoneum and in the spontaneous apoptosis of TGelicited neutrophils. The results showed that TG-elicited neutrophils (defined by flow cytometry as GR-1/Ly-6G hi cells) from normal (B6) and B6/ gld mice, but not from the Fas-deficient B6/lpr mice, express high levels of Fas. The TG-elicited neutrophil response began at 2 h, peaked at 4 h, and subsided by 24-48 h after TG administration in all three strains. However, the response was more prolonged in B6 mice, such that B6/gld and B6/lpr mice had fewer neutrophils at 6 h after TG administration than did B6 mice. Further studies showed that 4 h TG-elicited neutrophils from B6, B6/gld and B6/lpr mice undergo apoptosis in vitro at similar rates (as assessed through flow cytometry by the decrease in forward angle light-scatter and externalization of phosphatidylserine (PS; as detected by Annexin V-FITC) that occur as neutrophils undergo apoptosis). Fas expression was downregulated on apoptotic neutrophils in conjunction with maximal PS externalization and decreased forward angle light-scatter. Collectively, these findings suggest that FasL/Fas-mediated apoptosis is not essential in regulating the lifespan of neutrophils during an acute inflammatory response. The abbreviated inflammatory response observed in FasL/Fasdeficient mice is likely to be a secondary effect of the gld/lpr autoimmune/lymphoproliferative syndrome, and not a direct effect of FasL/Fas on the ability of inflammatory neutrophils to undergo apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fas ligand (gld)- and Fas (lpr)-deficient mice do not show alterations in the extravasation or apoptosis of inflammatory neutrophils

Fecho

Cohen

1998

Journal of Leukocyte Biology

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“…TNF-␣ has been variably reported either to induce, delay, or have no effect on neutrophil apoptosis (6,(23)(24)(25). These contrasting results could be explained, at least in part, by recent findings of Murray et al (26), who showed that although prolonged incubation (Ͼ18 h) of human neutrophils with TNF-␣ indeed causes a decrease in the extent of apoptosis, TNF-␣ can induce apoptosis in a proportion of cells at earlier times (Ͻ8 h).…”

Section: Promotion Of Neutrophil Apoptosis By Tnf-␣mentioning

confidence: 99%

Promotion of Neutrophil Apoptosis by TNF-α

Salamone

Giordano

Trevani

et al. 2001

The Journal of Immunology

110

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We examined the ability of TNF-α to modulate human neutrophil apoptosis. Neutrophils cultured with TNF-α alone undergo a low but significant increase in the number of apoptotic cells. More interestingly, when neutrophils were pretreated with TNF-α for 1–2 min at 37°C and then were exposed to a variety of agents such as immobilized IgG, IgG-coated erythrocytes, complement-treated erythrocytes, zymosan, PMA, zymosan-activated serum, fMLP, Escherichia coli, and GM-CSF for 3 h at 37°C, a marked stimulation of apoptosis was observed. Similar results were obtained in neutrophils pretreated with TNF-α for 30 min, 1 h, 3 h, and 18 h. Dose-dependent studies showed that TNF-α enhances neutrophil apoptosis at concentrations ranging from 1 to 100 ng/ml. In contrast to the observations made in neutrophils pretreated with TNF-α, there was no stimulation of apoptosis when TNF-α was added to neutrophils previously activated by conventional agonists. Experiments performed to establish the mechanism through which TNF-α promotes neutrophil apoptosis showed that neither reactive oxygen intermediates nor the Fas/Fas ligand system appear to be involved. Our results suggest that TNF-α plays a critical role in the control of neutrophil survival by virtue of its ability to induce an apoptotic death program which could be triggered by a variety of conventional agonists.

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“…The up-regulation of Fas on neutrophils from RSV þ NPA suggests that the accelerated neutrophil apoptosis may be mediated through a Fas pathway. TNF-a is one of the cytokines known to accelerate neutrophil apoptosis [25][26][27]. RSV-infected macrophages have been reported to produce TNF-a [28] and RSV infection of epithelial cells could release TNF receptor type I (TNF-RI) [29].…”

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confidence: 99%

The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)-induced bronchiolitis

Wang

Smith

Lovejoy

et al. 1998

Clinical and Experimental Immunology

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SUMMARYNeutrophils are the predominant inflammatory cell in the lung tissues and airways in RSV infection, and can augment the epithelial cell damage induced by RSV. Neutrophil apoptosis has been suggested to be a mechanism to reduce the potential for tissue injury. The apoptosis of neutrophils from nasopharyngeal aspirates (NPA) (n ¼ 19) and peripheral blood (PB) of infants with RSV bronchiolitis (n ¼ 11) and PB from healthy controls (n ¼ 9) was investigated. Monoclonal antibody against CD95 (Fas) and a binding protein Annexin V were used to determine the apoptosis of neutrophils. The expression of CD11b and CD18 on neutrophils was also detected with flow cytometry. The mean fluorescence intensity (MFI) of CD95 on neutrophils from RSV þ NPA was increased compared with cells from control PB (73·6 Ϯ 7·6 versus 31·5 Ϯ 4·3); the MFI of Annexin V, CD11b and CD18 on neutrophils from RSV þ NPA was upregulated compared with cells from both control PB (105·3 Ϯ 18·1 versus 11·8 Ϯ 1·5; 1683 Ϯ 153·3 versus 841·1 Ϯ 72·3; 517 Ϯ 50·5 versus 147 Ϯ 8·7, respectively) and RSV þ PB (105·3 Ϯ 18·1 versus 35·8 Ϯ 4·1; 1683 Ϯ 153·3 versus 818 Ϯ 141·2; 517 Ϯ 50·5 versus 260 Ϯ 25·8, respectively). Furthermore, the percentage of neutrophils expressing Annexin V and the MFI of CD18 on neutrophils from RSV þ PB were increased compared with neutrophils from control PB. In addition, both CD11b (MFI) and CD18 (MFI) correlated with Annexin V (MFI) on neutrophils. We conclude that neutrophil apoptosis in RSV bronchiolitis is accelerated; and CD11b/CD18 may play an important role in RSV infection by influencing neutrophil apoptosis.

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Rapid acceleration of neutrophil apoptosis by tumor necrosis factor-α

Cited by 140 publications

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Fas ligand (gld)- and Fas (lpr)-deficient mice do not show alterations in the extravasation or apoptosis of inflammatory neutrophils

Fas ligand (gld)- and Fas (lpr)-deficient mice do not show alterations in the extravasation or apoptosis of inflammatory neutrophils

Promotion of Neutrophil Apoptosis by TNF-α

The apoptosis of neutrophils is accelerated in respiratory syncytial virus (RSV)-induced bronchiolitis

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