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Random migration of polymorphonuclear leukocytes induced by GM‐CSF involving a signal transduction pathway different from that of fMLP
Author(s) -
Harakawa Nari,
Sasada Masataka,
Maeda Akinori,
Asagoe Kohsuke,
Nohgawa Masaharu,
Takano Kuniko,
Matsuda Yuzuru,
Yamamoto Kokichi,
Okuma Minoru
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.61.4.500
Subject(s) - chemotaxis , signal transduction , biology , protein kinase c , leukotriene b4 , phosphatidylinositol , n formylmethionine leucyl phenylalanine , kinase , microbiology and biotechnology , tyrosine kinase , granulocyte , immunology , biochemistry , inflammation , receptor
Granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) Induced random migration of human polymorphonuclear leukocytes (PMNs) but not chemotaxis. Chemoattractants such as N ‐formylmethionyl‐leucyl‐phenylalanine (fMLP), leukotriene B 4 (LTB 4 ), and interleukin‐8 (IL‐8) induced both random migration and chemotaxis. Other inflammatory cytokines, including granulocyte colony‐stimulating factor (G‐CSF), interleukin 1α (IL‐1α), and tumor necrosis factor α (TNF‐α), did not induce either movement. One‐minute exposure of PMNs to GM‐CSF was sufficient for the induction of random migration, whereas fMLP‐induced random migration required continued presence of fMLP. Inhibitors of phosphatidylinositol 3‐kinase (PI3‐K), protein kinase C (PKC), and protein tyrosine kinase (PTK) had no effect on random migration induced by GM‐CSF, whereas fMLP‐induced movements were partially inhibited by PTK inhibitors but not by inhibitors of PI3‐K inhibitors nor PKC inhibitors. Myosin light chain kinase inhibitors inhibited movements of PMNs induced by both GM‐CSF and fMLP. These findings also imply that some aspects of the signal transduction pathway of GM‐CSF leading to random migration is different from that of fMLP. Our findings suggest that cell movements are controlled through diverse signal transduction systems. J. Leukoc. Biol . 61: 500–506; 1997.