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Tumour necrosis factor-alpha-induced expression of intercellular adhesion molecule-1 on human eosinophilic leukaemia EoL-1 cells is mediated by the activation of nuclear factor-kappaB pathway.
Clin Exp Allergy. 2003 Feb; 33(2):241-8.CE

Abstract

BACKGROUND

Intercellular adhesion molecule-1 (ICAM-1) has been shown to mediate the adhesion and migration of eosinophils to the site of allergic inflammation. However, molecular mechanisms regulating the expression of ICAM-1 in eosinophils are still being elucidated. We investigated the effect of tumour necrosis factor-alpha (TNF-alpha) on ICAM-1 expression of eosinophils.

METHODS

The surface expression of ICAM-1 on a human eosinophilic leukaemic cell line, EoL-1, was assessed by immunocytochemical staining. The phosphorylation of inhibitor kappa B-alpha (IkappaB-alpha) and p38 mitogen-activated protein kinase (MAPK) was detected by Western blot. Nuclear factor kappa-B (NF-kappaB) pathway-related genes were evaluated by the cDNA expression array system, whereas the activity of NF-kappaB was measured by electrophoretic mobility shift assay (EMSA).

RESULTS

TNF-alpha was found to induce the cell surface expression of ICAM-1. A specific proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132), but not a p38 MAPK inhibitor (SB 203580), was found to suppress the TNF-alpha-induced expression of ICAM-1 on EoL-1 cells. The gene expressions of ICAM-1, NF-kappaB and IkappaBalpha were up-regulated after the stimulation with TNF-alpha. Further, TNF-alpha was shown to induce IkappaB-alpha phosphorylation and degradation, thereby indicating the activation of NF-kappaB. In EMSA, there was a shifted NF-kappaB band on TNF-alpha-treated cells with or without SB 203580, but no shifted band was observed on MG-132-treated cells.

CONCLUSION

In vitro studies of EoL-1 cells, an eosinophilic leukaemic cell line, confirmed that NF-kappaB plays an important role in the expression of ICAM-1 and recruitment of eosinophils in allergic inflammation.

Authors+Show Affiliations

Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., 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

12580918

Citation

Ip, W K., et al. "Tumour Necrosis Factor-alpha-induced Expression of Intercellular Adhesion Molecule-1 On Human Eosinophilic Leukaemia EoL-1 Cells Is Mediated By the Activation of Nuclear factor-kappaB Pathway." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 33, no. 2, 2003, pp. 241-8.
Ip WK, Wong CK, Lam CW. Tumour necrosis factor-alpha-induced expression of intercellular adhesion molecule-1 on human eosinophilic leukaemia EoL-1 cells is mediated by the activation of nuclear factor-kappaB pathway. Clin Exp Allergy. 2003;33(2):241-8.
Ip, W. K., Wong, C. K., & Lam, C. W. (2003). Tumour necrosis factor-alpha-induced expression of intercellular adhesion molecule-1 on human eosinophilic leukaemia EoL-1 cells is mediated by the activation of nuclear factor-kappaB pathway. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 33(2), 241-8.
Ip WK, Wong CK, Lam CW. Tumour Necrosis Factor-alpha-induced Expression of Intercellular Adhesion Molecule-1 On Human Eosinophilic Leukaemia EoL-1 Cells Is Mediated By the Activation of Nuclear factor-kappaB Pathway. Clin Exp Allergy. 2003;33(2):241-8. PubMed PMID: 12580918.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tumour necrosis factor-alpha-induced expression of intercellular adhesion molecule-1 on human eosinophilic leukaemia EoL-1 cells is mediated by the activation of nuclear factor-kappaB pathway. AU - Ip,W K, AU - Wong,C K, AU - Lam,C W K, PY - 2003/2/13/pubmed PY - 2003/4/15/medline PY - 2003/2/13/entrez SP - 241 EP - 8 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 33 IS - 2 N2 - BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) has been shown to mediate the adhesion and migration of eosinophils to the site of allergic inflammation. However, molecular mechanisms regulating the expression of ICAM-1 in eosinophils are still being elucidated. We investigated the effect of tumour necrosis factor-alpha (TNF-alpha) on ICAM-1 expression of eosinophils. METHODS: The surface expression of ICAM-1 on a human eosinophilic leukaemic cell line, EoL-1, was assessed by immunocytochemical staining. The phosphorylation of inhibitor kappa B-alpha (IkappaB-alpha) and p38 mitogen-activated protein kinase (MAPK) was detected by Western blot. Nuclear factor kappa-B (NF-kappaB) pathway-related genes were evaluated by the cDNA expression array system, whereas the activity of NF-kappaB was measured by electrophoretic mobility shift assay (EMSA). RESULTS: TNF-alpha was found to induce the cell surface expression of ICAM-1. A specific proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132), but not a p38 MAPK inhibitor (SB 203580), was found to suppress the TNF-alpha-induced expression of ICAM-1 on EoL-1 cells. The gene expressions of ICAM-1, NF-kappaB and IkappaBalpha were up-regulated after the stimulation with TNF-alpha. Further, TNF-alpha was shown to induce IkappaB-alpha phosphorylation and degradation, thereby indicating the activation of NF-kappaB. In EMSA, there was a shifted NF-kappaB band on TNF-alpha-treated cells with or without SB 203580, but no shifted band was observed on MG-132-treated cells. CONCLUSION: In vitro studies of EoL-1 cells, an eosinophilic leukaemic cell line, confirmed that NF-kappaB plays an important role in the expression of ICAM-1 and recruitment of eosinophils in allergic inflammation. SN - 0954-7894 UR - https://www.unboundmedicine.com/medline/citation/12580918/Tumour_necrosis_factor_alpha_induced_expression_of_intercellular_adhesion_molecule_1_on_human_eosinophilic_leukaemia_EoL_1_cells_is_mediated_by_the_activation_of_nuclear_factor_kappaB_pathway_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0954-7894&date=2003&volume=33&issue=2&spage=241 DB - PRIME DP - Unbound Medicine ER -