Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL): A Novel Mechanism of Antitumor Effect by Neutrophils

Yuhki Koga, Akinobu Matsuzaki, Aiko Suminoe, Hiroyoshi Hattori, Toshiro Hara

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

To detect the novel genes expressed uniquely in neutrophils and elucidate their function, the gene expression pattern was compared by using cDNA microarray containing 240 cytokine genes between the neutrophils and peripheral blood mononuclear cells (PBMCs) obtained from healthy human donors. Twenty-six genes, including tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), were expressed in neutrophils at a level >10 times higher than that seen in phytohemagglutinin-stimulated PBMCs. The amounts of mRNA and protein of TRAIL were quantified by real-time reverse transcription-PCR and ELISA, respectively. TRAIL was expressed in resting neutrophils at the mRNA and protein levels, and its expression was enhanced after stimulation with IFN-γ. Neutrophils expressed TRAIL on the cell surface and released it into the culture media. The cytotoxicity of neutrophil-derived TRAIL against Jurkat cells was determined by flow cytometry using FITC-conjugated annexin V. When Jurkat cells were cultured with neutrophils in the presence of IFN-γ, the number of Jurkat cells undergoing apoptosis increased, and such increase depended on the effector:target ratio. This cytotoxicity was suppressed partially by adding anti-TRAIL antibody to the media. Neutrophils may exert their own antitumor effect by TRAIL. A microarray analysis was found to be a useful tool for detecting novel genes that are suggested to play unknown roles in the neutrophil function.

Original languageEnglish
Pages (from-to)1037-1043
Number of pages7
JournalCancer Research
Volume64
Issue number3
DOIs
Publication statusPublished - Feb 1 2004

Fingerprint

TNF-Related Apoptosis-Inducing Ligand
Neutrophils
Jurkat Cells
Genes
Blood Cells
Apoptosis
Messenger RNA
Fluorescein-5-isothiocyanate
Annexin A5
Phytohemagglutinins
Microarray Analysis
Oligonucleotide Array Sequence Analysis
Reverse Transcription
Culture Media
Flow Cytometry
Proteins
Tumor Necrosis Factor-alpha
Enzyme-Linked Immunosorbent Assay
Cytokines
Gene Expression

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL) : A Novel Mechanism of Antitumor Effect by Neutrophils. / Koga, Yuhki; Matsuzaki, Akinobu; Suminoe, Aiko; Hattori, Hiroyoshi; Hara, Toshiro.

In: Cancer Research, Vol. 64, No. 3, 01.02.2004, p. 1037-1043.

Research output: Contribution to journalArticle

Koga, Yuhki ; Matsuzaki, Akinobu ; Suminoe, Aiko ; Hattori, Hiroyoshi ; Hara, Toshiro. / Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL) : A Novel Mechanism of Antitumor Effect by Neutrophils. In: Cancer Research. 2004 ; Vol. 64, No. 3. pp. 1037-1043.
@article{e061260264c0461ea15314824ebb8b27,
title = "Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL): A Novel Mechanism of Antitumor Effect by Neutrophils",
abstract = "To detect the novel genes expressed uniquely in neutrophils and elucidate their function, the gene expression pattern was compared by using cDNA microarray containing 240 cytokine genes between the neutrophils and peripheral blood mononuclear cells (PBMCs) obtained from healthy human donors. Twenty-six genes, including tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), were expressed in neutrophils at a level >10 times higher than that seen in phytohemagglutinin-stimulated PBMCs. The amounts of mRNA and protein of TRAIL were quantified by real-time reverse transcription-PCR and ELISA, respectively. TRAIL was expressed in resting neutrophils at the mRNA and protein levels, and its expression was enhanced after stimulation with IFN-γ. Neutrophils expressed TRAIL on the cell surface and released it into the culture media. The cytotoxicity of neutrophil-derived TRAIL against Jurkat cells was determined by flow cytometry using FITC-conjugated annexin V. When Jurkat cells were cultured with neutrophils in the presence of IFN-γ, the number of Jurkat cells undergoing apoptosis increased, and such increase depended on the effector:target ratio. This cytotoxicity was suppressed partially by adding anti-TRAIL antibody to the media. Neutrophils may exert their own antitumor effect by TRAIL. A microarray analysis was found to be a useful tool for detecting novel genes that are suggested to play unknown roles in the neutrophil function.",
author = "Yuhki Koga and Akinobu Matsuzaki and Aiko Suminoe and Hiroyoshi Hattori and Toshiro Hara",
year = "2004",
month = "2",
day = "1",
doi = "10.1158/0008-5472.CAN-03-1808",
language = "English",
volume = "64",
pages = "1037--1043",
journal = "Cancer Research",
issn = "0008-5472",
number = "3",

}

TY - JOUR

T1 - Neutrophil-Derived TNF-Related Apoptosis-Inducing Ligand (TRAIL)

T2 - A Novel Mechanism of Antitumor Effect by Neutrophils

AU - Koga, Yuhki

AU - Matsuzaki, Akinobu

AU - Suminoe, Aiko

AU - Hattori, Hiroyoshi

AU - Hara, Toshiro

PY - 2004/2/1

Y1 - 2004/2/1

N2 - To detect the novel genes expressed uniquely in neutrophils and elucidate their function, the gene expression pattern was compared by using cDNA microarray containing 240 cytokine genes between the neutrophils and peripheral blood mononuclear cells (PBMCs) obtained from healthy human donors. Twenty-six genes, including tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), were expressed in neutrophils at a level >10 times higher than that seen in phytohemagglutinin-stimulated PBMCs. The amounts of mRNA and protein of TRAIL were quantified by real-time reverse transcription-PCR and ELISA, respectively. TRAIL was expressed in resting neutrophils at the mRNA and protein levels, and its expression was enhanced after stimulation with IFN-γ. Neutrophils expressed TRAIL on the cell surface and released it into the culture media. The cytotoxicity of neutrophil-derived TRAIL against Jurkat cells was determined by flow cytometry using FITC-conjugated annexin V. When Jurkat cells were cultured with neutrophils in the presence of IFN-γ, the number of Jurkat cells undergoing apoptosis increased, and such increase depended on the effector:target ratio. This cytotoxicity was suppressed partially by adding anti-TRAIL antibody to the media. Neutrophils may exert their own antitumor effect by TRAIL. A microarray analysis was found to be a useful tool for detecting novel genes that are suggested to play unknown roles in the neutrophil function.

AB - To detect the novel genes expressed uniquely in neutrophils and elucidate their function, the gene expression pattern was compared by using cDNA microarray containing 240 cytokine genes between the neutrophils and peripheral blood mononuclear cells (PBMCs) obtained from healthy human donors. Twenty-six genes, including tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), were expressed in neutrophils at a level >10 times higher than that seen in phytohemagglutinin-stimulated PBMCs. The amounts of mRNA and protein of TRAIL were quantified by real-time reverse transcription-PCR and ELISA, respectively. TRAIL was expressed in resting neutrophils at the mRNA and protein levels, and its expression was enhanced after stimulation with IFN-γ. Neutrophils expressed TRAIL on the cell surface and released it into the culture media. The cytotoxicity of neutrophil-derived TRAIL against Jurkat cells was determined by flow cytometry using FITC-conjugated annexin V. When Jurkat cells were cultured with neutrophils in the presence of IFN-γ, the number of Jurkat cells undergoing apoptosis increased, and such increase depended on the effector:target ratio. This cytotoxicity was suppressed partially by adding anti-TRAIL antibody to the media. Neutrophils may exert their own antitumor effect by TRAIL. A microarray analysis was found to be a useful tool for detecting novel genes that are suggested to play unknown roles in the neutrophil function.

UR - http://www.scopus.com/inward/record.url?scp=0842325792&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0842325792&partnerID=8YFLogxK

U2 - 10.1158/0008-5472.CAN-03-1808

DO - 10.1158/0008-5472.CAN-03-1808

M3 - Article

C2 - 14871835

AN - SCOPUS:0842325792

VL - 64

SP - 1037

EP - 1043

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 3

ER -