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Random migration of polymorphonuclear leukocytes induced by GM-CSF involving a signal transduction pathway different
N Harakawa1, M Sasada, A Maeda
1Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Japan.
Abstract:
Granulocyte-macrophage colony-stimulating factor (GM-CSF) induced random migration of human polymorphonuclear leukocytes (PMNs) but not chemotaxis. Chemoattractants such as N-formyl-methionyl-leucyl-phenylalanine (fMLP), leukotriene B4 (LTB4), and interleukin-8 (IL-8) induced both random migration and chemotaxis. Other inflammatory cytokines, including granulocyte colony-stimulating factor (G-CSF), interleukin 1alpha (IL-1alpha), and tumor necrosis factor alpha (TNF-alpha), 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.
Insights
Granulocyte-macrophage colony-stimulating factor (GM-CSF) triggers random migration in human white blood cells (PMNs), but not directed movement. This contrasts with other chemoattractants, highlighting diverse cell signaling pathways.
Area of Science:
- Immunology
- Cell Biology
- Signal Transduction
Background:
- Human polymorphonuclear leukocytes (PMNs) are crucial for immune responses.
- Cell migration, including random migration and chemotaxis, is vital for immune cell function.
- Understanding the signaling pathways that control PMN migration is essential for developing targeted therapies.
Purpose of the Study:
- To investigate the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on PMN migration.
- To compare the signaling pathways induced by GM-CSF with those of known chemoattractants like N-formyl-methionyl-leucyl-phenylalanine (fMLP).
- To elucidate the distinct mechanisms governing random migration and chemotaxis.
Main Methods:
- Exposure of PMNs to GM-CSF, fMLP, and other cytokines.
- Assessment of random migration and chemotaxis.
- Inhibition studies using specific pathway inhibitors (PI3-K, PKC, PTK, MLCK).
Main Results:
- GM-CSF induced random migration but not chemotaxis in PMNs.
- fMLP, leukotriene B4 (LTB4), and interleukin-8 (IL-8) induced both random migration and chemotaxis.
- GM-CSF-induced migration was unaffected by PI3-K, PKC, and PTK inhibitors, unlike fMLP-induced migration.
- Myosin light chain kinase inhibitors affected migration induced by both GM-CSF and fMLP.
- Distinct signal transduction pathways are involved in GM-CSF and fMLP-mediated PMN migration.
Conclusions:
- GM-CSF and fMLP utilize different signaling pathways to induce PMN migration.
- PMN movement is regulated by diverse intracellular signaling systems.
- These findings contribute to understanding the complexity of immune cell trafficking and response.
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