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Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor-induced adhesion molecule expression on eosinophils by p38 mitogen-activated protein kinase and nuclear factor-[kappa] B.
Am J Respir Cell Mol Biol. 2003 Jul; 29(1):133-47.AJ

Abstract

We investigated the intracellular signaling mechanisms for cytokine interleukin (IL)-3, IL-5, or granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced expression of adhesion molecules including very late antigen 4 (CD49 d), macrophage antigen-1 (CD11b), leukocyte function-associated antigen-1 (CD11a/CD18), intercellular adhesion molecule (ICAM)-1, and ICAM-3 on eosinophils. The expression of adhesion molecules and nuclear factor (NF)-kappaB pathway was measured by flow cytometry and cDNA expression array, respectively. The phosphorylation of inhibitor kappaB-alpha and p38 mitogen-activated protein kinase (MAPK) was detected by Western blot, whereas NF-kappaB activity was measured by electrophoretic mobility shift assay. IL-3, IL-5, and GM-CSF could enhance p38 MAPK and NF-kappaB activity and induce ICAM-1, CD11b, and CD18 expressions on eosinophils. They could suppress ICAM-3 expression, but had no effect on CD49 d expression. Either SB 203580 or MG-132 was able to offset the cytokine-induced expression of ICAM-1. Only SB 203580 could reverse the effect on CD11b, CD18, and ICAM-3 expressions. Therefore, the expression of ICAM-1 might involve both p38 MAPK and NF-kappaB activities, whereas the regulation of CD11b, CD18, and ICAM-3 expressions might be mediated through p38 MAPK but not NF-kappaB. These cytokines therefore play a crucial role, via the p38 MAPK and NF-kappaB pathways, in the expression of important adhesion molecules on eosinophils in allergic inflammation.

Authors+Show Affiliations

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

Pub Type(s)

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

Language

eng

PubMed ID

12600815

Citation

Wong, Chun K., et al. "Interleukin-3, -5, and Granulocyte Macrophage Colony-stimulating Factor-induced Adhesion Molecule Expression On Eosinophils By P38 Mitogen-activated Protein Kinase and Nuclear Factor-[kappa] B." American Journal of Respiratory Cell and Molecular Biology, vol. 29, no. 1, 2003, pp. 133-47.
Wong CK, Ip WK, Lam CW. Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor-induced adhesion molecule expression on eosinophils by p38 mitogen-activated protein kinase and nuclear factor-[kappa] B. Am J Respir Cell Mol Biol. 2003;29(1):133-47.
Wong, C. K., Ip, W. K., & Lam, C. W. (2003). Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor-induced adhesion molecule expression on eosinophils by p38 mitogen-activated protein kinase and nuclear factor-[kappa] B. American Journal of Respiratory Cell and Molecular Biology, 29(1), 133-47.
Wong CK, Ip WK, Lam CW. Interleukin-3, -5, and Granulocyte Macrophage Colony-stimulating Factor-induced Adhesion Molecule Expression On Eosinophils By P38 Mitogen-activated Protein Kinase and Nuclear Factor-[kappa] B. Am J Respir Cell Mol Biol. 2003;29(1):133-47. PubMed PMID: 12600815.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-3, -5, and granulocyte macrophage colony-stimulating factor-induced adhesion molecule expression on eosinophils by p38 mitogen-activated protein kinase and nuclear factor-[kappa] B. AU - Wong,Chun K, AU - Ip,Wai K, AU - Lam,Christopher W K, Y1 - 2003/02/14/ PY - 2003/2/26/pubmed PY - 2003/8/6/medline PY - 2003/2/26/entrez SP - 133 EP - 47 JF - American journal of respiratory cell and molecular biology JO - Am J Respir Cell Mol Biol VL - 29 IS - 1 N2 - We investigated the intracellular signaling mechanisms for cytokine interleukin (IL)-3, IL-5, or granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced expression of adhesion molecules including very late antigen 4 (CD49 d), macrophage antigen-1 (CD11b), leukocyte function-associated antigen-1 (CD11a/CD18), intercellular adhesion molecule (ICAM)-1, and ICAM-3 on eosinophils. The expression of adhesion molecules and nuclear factor (NF)-kappaB pathway was measured by flow cytometry and cDNA expression array, respectively. The phosphorylation of inhibitor kappaB-alpha and p38 mitogen-activated protein kinase (MAPK) was detected by Western blot, whereas NF-kappaB activity was measured by electrophoretic mobility shift assay. IL-3, IL-5, and GM-CSF could enhance p38 MAPK and NF-kappaB activity and induce ICAM-1, CD11b, and CD18 expressions on eosinophils. They could suppress ICAM-3 expression, but had no effect on CD49 d expression. Either SB 203580 or MG-132 was able to offset the cytokine-induced expression of ICAM-1. Only SB 203580 could reverse the effect on CD11b, CD18, and ICAM-3 expressions. Therefore, the expression of ICAM-1 might involve both p38 MAPK and NF-kappaB activities, whereas the regulation of CD11b, CD18, and ICAM-3 expressions might be mediated through p38 MAPK but not NF-kappaB. These cytokines therefore play a crucial role, via the p38 MAPK and NF-kappaB pathways, in the expression of important adhesion molecules on eosinophils in allergic inflammation. SN - 1044-1549 UR - https://www.unboundmedicine.com/medline/citation/12600815/Interleukin_3__5_and_granulocyte_macrophage_colony_stimulating_factor_induced_adhesion_molecule_expression_on_eosinophils_by_p38_mitogen_activated_protein_kinase_and_nuclear_factor_[kappa]_B_ L2 - https://www.atsjournals.org/doi/10.1165/rcmb.2002-0289OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -