Administration of granulocyte colony-stimulating factor induces hyporesponsiveness to lipopolysaccharide and impairs antigen-presenting function of peripheral blood monocytes

Kazutaka Sunami, Takanori Teshima, Yuichiro Nawa, Yasushi Hiramatsu, Yoshinobu Maeda, Katsuto Takenaka, Katsuji Shinagawa, Fumihiko Ishimaru, Kazuma Ikeda, Kenji Niiya, Mine Harada

Research output: Contribution to journalArticle

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Abstract

Objective. The incidence and severity of acute graft-vs-host disease after allogeneic transplantation of granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood stem cells (PBSC) are not greater than those after conventional bone marrow transplantation despite infusion of more than one log greater number of donor T cells in PBSC. It has been postulated that monocytes from G-CSF-mobilized donors suppress alloreactivity of donor T cells. Materials and Methods. We investigated the phenotype and function of monocytes in normal individuals receiving 10 μg/kg of G-CSF for 4 days. Results. Monocytes were phenotypically and functionally different after G-CSF administration from steady-state monocytes. They were characterized by an increased CD14+CD16+ subpopulation, reduced expression of HLA-DR, and diminished ability to produce tumor necrosis factor-α and interleukin-10 to lipopolysaccharide, compared with steady-state monocytes. These alterations were not replicated by culturing monocytes with G-CSF in vitro, suggesting an indirect effect of G-CSF. In addition, the antigen-presenting function of G-CSF-mobilized monocytes was impaired. Conclusion. Hyporesponsiveness of G-CSF-treated monocytes to lipopolysaccharide with regard to tumor necrosis factor-α production, together with impaired antigen-presenting function, may be responsible for the unexpectedly low incidence of graft-vs-host disease after G-CSF-mobilized PBSC transplantation.

Original languageEnglish
Pages (from-to)1117-1124
Number of pages8
JournalExperimental Hematology
Volume29
Issue number9
DOIs
Publication statusPublished - Jan 1 2001

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Granulocyte Colony-Stimulating Factor
Lipopolysaccharides
Monocytes
Antigens
Graft vs Host Disease
Tumor Necrosis Factor-alpha
T-Lymphocytes
Peripheral Blood Stem Cell Transplantation
Incidence
Homologous Transplantation
HLA-DR Antigens
Bone Marrow Transplantation
Interleukin-10
Phenotype

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Hematology
  • Genetics
  • Cell Biology
  • Cancer Research

Cite this

Administration of granulocyte colony-stimulating factor induces hyporesponsiveness to lipopolysaccharide and impairs antigen-presenting function of peripheral blood monocytes. / Sunami, Kazutaka; Teshima, Takanori; Nawa, Yuichiro; Hiramatsu, Yasushi; Maeda, Yoshinobu; Takenaka, Katsuto; Shinagawa, Katsuji; Ishimaru, Fumihiko; Ikeda, Kazuma; Niiya, Kenji; Harada, Mine.

In: Experimental Hematology, Vol. 29, No. 9, 01.01.2001, p. 1117-1124.

Research output: Contribution to journalArticle

Sunami, K, Teshima, T, Nawa, Y, Hiramatsu, Y, Maeda, Y, Takenaka, K, Shinagawa, K, Ishimaru, F, Ikeda, K, Niiya, K & Harada, M 2001, 'Administration of granulocyte colony-stimulating factor induces hyporesponsiveness to lipopolysaccharide and impairs antigen-presenting function of peripheral blood monocytes', Experimental Hematology, vol. 29, no. 9, pp. 1117-1124. https://doi.org/10.1016/S0301-472X(01)00679-8
Sunami, Kazutaka ; Teshima, Takanori ; Nawa, Yuichiro ; Hiramatsu, Yasushi ; Maeda, Yoshinobu ; Takenaka, Katsuto ; Shinagawa, Katsuji ; Ishimaru, Fumihiko ; Ikeda, Kazuma ; Niiya, Kenji ; Harada, Mine. / Administration of granulocyte colony-stimulating factor induces hyporesponsiveness to lipopolysaccharide and impairs antigen-presenting function of peripheral blood monocytes. In: Experimental Hematology. 2001 ; Vol. 29, No. 9. pp. 1117-1124.
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AU - Sunami, Kazutaka

AU - Teshima, Takanori

AU - Nawa, Yuichiro

AU - Hiramatsu, Yasushi

AU - Maeda, Yoshinobu

AU - Takenaka, Katsuto

AU - Shinagawa, Katsuji

AU - Ishimaru, Fumihiko

AU - Ikeda, Kazuma

AU - Niiya, Kenji

AU - Harada, Mine

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N2 - Objective. The incidence and severity of acute graft-vs-host disease after allogeneic transplantation of granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood stem cells (PBSC) are not greater than those after conventional bone marrow transplantation despite infusion of more than one log greater number of donor T cells in PBSC. It has been postulated that monocytes from G-CSF-mobilized donors suppress alloreactivity of donor T cells. Materials and Methods. We investigated the phenotype and function of monocytes in normal individuals receiving 10 μg/kg of G-CSF for 4 days. Results. Monocytes were phenotypically and functionally different after G-CSF administration from steady-state monocytes. They were characterized by an increased CD14+CD16+ subpopulation, reduced expression of HLA-DR, and diminished ability to produce tumor necrosis factor-α and interleukin-10 to lipopolysaccharide, compared with steady-state monocytes. These alterations were not replicated by culturing monocytes with G-CSF in vitro, suggesting an indirect effect of G-CSF. In addition, the antigen-presenting function of G-CSF-mobilized monocytes was impaired. Conclusion. Hyporesponsiveness of G-CSF-treated monocytes to lipopolysaccharide with regard to tumor necrosis factor-α production, together with impaired antigen-presenting function, may be responsible for the unexpectedly low incidence of graft-vs-host disease after G-CSF-mobilized PBSC transplantation.

AB - Objective. The incidence and severity of acute graft-vs-host disease after allogeneic transplantation of granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood stem cells (PBSC) are not greater than those after conventional bone marrow transplantation despite infusion of more than one log greater number of donor T cells in PBSC. It has been postulated that monocytes from G-CSF-mobilized donors suppress alloreactivity of donor T cells. Materials and Methods. We investigated the phenotype and function of monocytes in normal individuals receiving 10 μg/kg of G-CSF for 4 days. Results. Monocytes were phenotypically and functionally different after G-CSF administration from steady-state monocytes. They were characterized by an increased CD14+CD16+ subpopulation, reduced expression of HLA-DR, and diminished ability to produce tumor necrosis factor-α and interleukin-10 to lipopolysaccharide, compared with steady-state monocytes. These alterations were not replicated by culturing monocytes with G-CSF in vitro, suggesting an indirect effect of G-CSF. In addition, the antigen-presenting function of G-CSF-mobilized monocytes was impaired. Conclusion. Hyporesponsiveness of G-CSF-treated monocytes to lipopolysaccharide with regard to tumor necrosis factor-α production, together with impaired antigen-presenting function, may be responsible for the unexpectedly low incidence of graft-vs-host disease after G-CSF-mobilized PBSC transplantation.

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