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Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor induce adhesion and chemotaxis of human eosinophils via p38 mitogen-activated protein kinase and nuclear factor kappaB.
Immunopharmacol Immunotoxicol. 2005; 27(3):371-93.II

Abstract

Hematopoietic cytokines such as interleukin (IL)-3, IL-5, and granulocyte macrophage colony-stimulating factor (GM-CSF) play a fundamental role in eosinophil functions in allergic asthma. The intracellular signal transduction mechanisms of these cytokines regulating the activation of eosinophils have been potential therapeutic targets. We investigated the roles of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-kappaB) in IL-3, IL-5, and GM-CSF-induced adhesion, morphological changes, and subsequence transmigration of human eosinophils. IL-3, IL-5, and GM-CSF could augment the phosphorylation of p38 MAPK and nucleus translocation of NF-kappaB in eosinophils. cDNA expression arrays demonstrated that the gene expression levels of several adhesion molecules including intercellular adhesion molecule-1 (ICAM-1), alpha6, beta2 integrin (CD18), and CD44 were upregulated by these cytokines. Results from functional assays showed that adhesion of eosinophils onto airway epithelial cells was enhanced after IL-3 and IL-5 but not GM-CSF stimulation. These cytokines could markedly induce shape change and augment the transmigration of eosinophils. Moreover, administration of either p38 MAPK inhibitor, SB 203580, or proteasome inhibitor, N-cbz-Leu-Leu-leucinal (MG-132), could inhibit the cytokine-induced adhesion, shape change, and transmigration of eosinophils. Together, our findings suggest that IL-3, IL-5, and GM-CSF regulated the adhesion and chemotaxis of human eosinophils through shared signaling pathways involving both p38 MAPK and NF-kappaB. Our results therefore shed light on the further development of more effective agents for allergic and inflammatory diseases.

Authors+Show Affiliations

Department of Chemical Pathology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16237950

Citation

Ip, Wai Ki, et al. "Interleukin-3, -5, and Granulocyte Macrophage Colony-stimulating Factor Induce Adhesion and Chemotaxis of Human Eosinophils Via P38 Mitogen-activated Protein Kinase and Nuclear Factor KappaB." Immunopharmacology and Immunotoxicology, vol. 27, no. 3, 2005, pp. 371-93.
Ip WK, Wong CK, Wang CB, et al. Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor induce adhesion and chemotaxis of human eosinophils via p38 mitogen-activated protein kinase and nuclear factor kappaB. Immunopharmacol Immunotoxicol. 2005;27(3):371-93.
Ip, W. K., Wong, C. K., Wang, C. B., Tian, Y. P., & Lam, C. W. (2005). Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor induce adhesion and chemotaxis of human eosinophils via p38 mitogen-activated protein kinase and nuclear factor kappaB. Immunopharmacology and Immunotoxicology, 27(3), 371-93.
Ip WK, et al. Interleukin-3, -5, and Granulocyte Macrophage Colony-stimulating Factor Induce Adhesion and Chemotaxis of Human Eosinophils Via P38 Mitogen-activated Protein Kinase and Nuclear Factor KappaB. Immunopharmacol Immunotoxicol. 2005;27(3):371-93. PubMed PMID: 16237950.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor induce adhesion and chemotaxis of human eosinophils via p38 mitogen-activated protein kinase and nuclear factor kappaB. AU - Ip,Wai Ki, AU - Wong,Chun Kwok, AU - Wang,Cheng Bin, AU - Tian,Ya Ping, AU - Lam,Christopher Wai Kei, PY - 2005/10/22/pubmed PY - 2005/12/16/medline PY - 2005/10/22/entrez SP - 371 EP - 93 JF - Immunopharmacology and immunotoxicology JO - Immunopharmacol Immunotoxicol VL - 27 IS - 3 N2 - Hematopoietic cytokines such as interleukin (IL)-3, IL-5, and granulocyte macrophage colony-stimulating factor (GM-CSF) play a fundamental role in eosinophil functions in allergic asthma. The intracellular signal transduction mechanisms of these cytokines regulating the activation of eosinophils have been potential therapeutic targets. We investigated the roles of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-kappaB) in IL-3, IL-5, and GM-CSF-induced adhesion, morphological changes, and subsequence transmigration of human eosinophils. IL-3, IL-5, and GM-CSF could augment the phosphorylation of p38 MAPK and nucleus translocation of NF-kappaB in eosinophils. cDNA expression arrays demonstrated that the gene expression levels of several adhesion molecules including intercellular adhesion molecule-1 (ICAM-1), alpha6, beta2 integrin (CD18), and CD44 were upregulated by these cytokines. Results from functional assays showed that adhesion of eosinophils onto airway epithelial cells was enhanced after IL-3 and IL-5 but not GM-CSF stimulation. These cytokines could markedly induce shape change and augment the transmigration of eosinophils. Moreover, administration of either p38 MAPK inhibitor, SB 203580, or proteasome inhibitor, N-cbz-Leu-Leu-leucinal (MG-132), could inhibit the cytokine-induced adhesion, shape change, and transmigration of eosinophils. Together, our findings suggest that IL-3, IL-5, and GM-CSF regulated the adhesion and chemotaxis of human eosinophils through shared signaling pathways involving both p38 MAPK and NF-kappaB. Our results therefore shed light on the further development of more effective agents for allergic and inflammatory diseases. SN - 0892-3973 UR - https://www.unboundmedicine.com/medline/citation/16237950/Interleukin_3__5_and_granulocyte_macrophage_colony_stimulating_factor_induce_adhesion_and_chemotaxis_of_human_eosinophils_via_p38_mitogen_activated_protein_kinase_and_nuclear_factor_kappaB_ L2 - https://www.tandfonline.com/doi/full/10.1080/08923970500240925 DB - PRIME DP - Unbound Medicine ER -