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Enhanced mobilization of hematopoietic progenitor cells by mouse MIP‐2 and granulocyte colony‐stimulating factor in mice
Author(s) -
Wang Jianbin,
Mukaida Naofumi,
Zhang Yi,
Lto Takaaki,
Nakao Shinji,
Matsushima Kouji
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.62.4.503
Subject(s) - haematopoiesis , biology , bone marrow , progenitor cell , chemokine , granulocyte , mobilization , immunology , neutrophil elastase , stromal cell , myeloid , granulocyte colony stimulating factor , macrophage , granulocyte macrophage colony stimulating factor , microbiology and biotechnology , cytokine , stem cell , inflammation , cancer research , biochemistry , in vitro , history , genetics , archaeology , chemotherapy
Abstract Human interleukin‐8 (IL‐8) induces a rapid mobilization of hematopoietic progenitor cells (HPCs) into peripheral blood in mice and primates. Because an exact homologue of human IL‐8 does not exist in mice, a chemokine, macrophage inflammatory protein‐2 (MIP‐2), is supposed to substitute the function of IL‐8 in mice. Hence, we investigated the capacity of mouse MIP‐2 to induce HPC mobilization in mice. Mouse MIP‐2 induced, in either untreated or splenectomized mice, a rapid HPC mobilization, as evidenced by increased numbers of colony‐forming unit granulocyte‐macrophage (CFU‐GM) and lineage marker (Lin) ‐ c‐kit + Sca‐1 + cells. Although release of elastase from activated neutrophils was proposed to be involved in IL‐8‐induced HPC mobilization, mouse MIP‐2 induced similar levels of HPC mobilization in elastase‐deficient beige mice at a similar level to normal ones. This HPC mobilization by MIP‐2 was markedly enhanced by pretreatment with granulocyte‐colony‐stimulating factor (G‐CSF). Moreover, the combination of G‐CSF and MIP‐2 apparently down‐regulated L‐selectin expression on Lin ‐ Sca‐1 + cells in peripheral blood as well as bone marrow. Thus, MIP‐2 may down‐modulate the interaction between HPCs and bone marrow stroma by reducing L‐selectin expression on HPCs and cause rapid mobilization of HPCs into peripheral blood. J. Leukoc. Biol. 62: 503–509; 1997.