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Pathways for eosinophil lipid body induction: differing signal transduction in cells from normal and hypereosinophilic subjects.
J Leukoc Biol. 1998 Oct; 64(4):563-9.JL

Abstract

Although lipid bodies, inducible cytoplasmic inclusions active in arachidonic acid metabolism, are abundant in activated leukocytes, including eosinophils, mechanisms for eosinophil lipid body formation are not certain. Eosinophils from hypereosinophilic syndrome (HES) donors contained about twice (approximately 18/cell) as many lipid bodies as eosinophils froin normal donors (approximately 10/cell). By immunocytochemistry both 5- and 15-lipoxygenases were localized at lipid bodies in HES eosinophils. Platelet-activating factor (PAF) induced rapid, receptor-mediated increases in lipid bodies in normal and HES eosinophils. Protein kinase C (PKC) inhibitors, chelerythrine and calphostin C, inhibited PAF-induced lipid body formation partially in normal and HES eosinophils. In HES, but not normal, eosinophils, PAF-induced lipid body formation was completely blocked by two tyrosine kinase inhibitors, herbimycin A and genistein, which were not acting on 5-lipoxygenase because they also blocked 5-HETE-induced lipid body formation in HES, and not normal, eosinophils. After 24 h culture with eosinophil growth factor cytokines [interleukin (IL)-3, IL-5, and granulocyte-macrophage colony-stimulating factor (GM-CSF) or GM-CSF alone but not IL-5 or IL-3 alone], normal eosinophils were induced to exhibit an HES-like phenotype, including increased lipid body numbers and tyrosine kinase-dependent signaling for PAF-induced lipid body formation. Thus, signal transduction mechanisms involved in PAF-induced lipid body formation in eosinophils can be differentially recruited. Tyrosine kinase-dependent signaling is not involved in normal eosinophils, but is active in HES eosinophils and in normal eosinophils cultured with GM-CSF. PKC- and tyrosine kinase-dependent pathways are involved in the formation of eosinophil lipid bodies, which may facilitate enhanced synthesis of lipoxygenase-derived eicosanoids.

Authors+Show Affiliations

Charles A. Dana Research Institute, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9766638

Citation

Bozza, P T., et al. "Pathways for Eosinophil Lipid Body Induction: Differing Signal Transduction in Cells From Normal and Hypereosinophilic Subjects." Journal of Leukocyte Biology, vol. 64, no. 4, 1998, pp. 563-9.
Bozza PT, Yu W, Cassara J, et al. Pathways for eosinophil lipid body induction: differing signal transduction in cells from normal and hypereosinophilic subjects. J Leukoc Biol. 1998;64(4):563-9.
Bozza, P. T., Yu, W., Cassara, J., & Weller, P. F. (1998). Pathways for eosinophil lipid body induction: differing signal transduction in cells from normal and hypereosinophilic subjects. Journal of Leukocyte Biology, 64(4), 563-9.
Bozza PT, et al. Pathways for Eosinophil Lipid Body Induction: Differing Signal Transduction in Cells From Normal and Hypereosinophilic Subjects. J Leukoc Biol. 1998;64(4):563-9. PubMed PMID: 9766638.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathways for eosinophil lipid body induction: differing signal transduction in cells from normal and hypereosinophilic subjects. AU - Bozza,P T, AU - Yu,W, AU - Cassara,J, AU - Weller,P F, PY - 1998/10/10/pubmed PY - 1998/10/10/medline PY - 1998/10/10/entrez SP - 563 EP - 9 JF - Journal of leukocyte biology JO - J Leukoc Biol VL - 64 IS - 4 N2 - Although lipid bodies, inducible cytoplasmic inclusions active in arachidonic acid metabolism, are abundant in activated leukocytes, including eosinophils, mechanisms for eosinophil lipid body formation are not certain. Eosinophils from hypereosinophilic syndrome (HES) donors contained about twice (approximately 18/cell) as many lipid bodies as eosinophils froin normal donors (approximately 10/cell). By immunocytochemistry both 5- and 15-lipoxygenases were localized at lipid bodies in HES eosinophils. Platelet-activating factor (PAF) induced rapid, receptor-mediated increases in lipid bodies in normal and HES eosinophils. Protein kinase C (PKC) inhibitors, chelerythrine and calphostin C, inhibited PAF-induced lipid body formation partially in normal and HES eosinophils. In HES, but not normal, eosinophils, PAF-induced lipid body formation was completely blocked by two tyrosine kinase inhibitors, herbimycin A and genistein, which were not acting on 5-lipoxygenase because they also blocked 5-HETE-induced lipid body formation in HES, and not normal, eosinophils. After 24 h culture with eosinophil growth factor cytokines [interleukin (IL)-3, IL-5, and granulocyte-macrophage colony-stimulating factor (GM-CSF) or GM-CSF alone but not IL-5 or IL-3 alone], normal eosinophils were induced to exhibit an HES-like phenotype, including increased lipid body numbers and tyrosine kinase-dependent signaling for PAF-induced lipid body formation. Thus, signal transduction mechanisms involved in PAF-induced lipid body formation in eosinophils can be differentially recruited. Tyrosine kinase-dependent signaling is not involved in normal eosinophils, but is active in HES eosinophils and in normal eosinophils cultured with GM-CSF. PKC- and tyrosine kinase-dependent pathways are involved in the formation of eosinophil lipid bodies, which may facilitate enhanced synthesis of lipoxygenase-derived eicosanoids. SN - 0741-5400 UR - https://www.unboundmedicine.com/medline/citation/9766638/Pathways_for_eosinophil_lipid_body_induction:_differing_signal_transduction_in_cells_from_normal_and_hypereosinophilic_subjects_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0741-5400&date=1998&volume=64&issue=4&spage=563 DB - PRIME DP - Unbound Medicine ER -