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Induction of adhesion molecules upon the interaction between eosinophils and bronchial epithelial cells: involvement of p38 MAPK and NF-kappaB.
Int Immunopharmacol. 2006 Dec 05; 6(12):1859-71.II

Abstract

Eosinophils are principal effector cells of inflammation in allergic asthma, characterized by their infiltration and accumulation at inflammatory sites mediated by chemokine eotaxin, and interaction with adhesion molecules expressed on bronchial epithelial cells. In this study, tumor necrosis factor (TNF)-alpha and/or the interaction of eosinophils and bronchial epithelial BEAS-2B cells were found to up-regulate the cell surface expression of adhesion molecules intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 on BEAS-2B cells, and ICAM-1 and leukocyte function-associated antigen-1 (LFA-1) on eosinophils. Interaction of eosinophils and BEAS-2B cells could induce the release of granulocyte macrophage colony-stimulating factor (GM-CSF) and activate both p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB activities in BEAS-2B cells but only NF-kappaB activity in eosinophils. Both proteasome inhibitor MG-132 and selective p38 MAPK inhibitor SB 203580 could significantly decrease the expression of ICAM-1 on BEAS-2B cells and CD18 on eosinophils upon co-culture with or without TNF-alpha treatment. However, the expression of VCAM-1 on BEAS-2B cells was only up-regulated by TNF-alpha-induced NF-kappaB activity. The interaction of eosinophils and bronchial epithelial cells therefore plays an important role in the up-regulation of adhesion molecules on eosinophils and epithelial cells via differential intracellular signalling pathways during 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 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

17052676

Citation

Wong, C K., et al. "Induction of Adhesion Molecules Upon the Interaction Between Eosinophils and Bronchial Epithelial Cells: Involvement of P38 MAPK and NF-kappaB." International Immunopharmacology, vol. 6, no. 12, 2006, pp. 1859-71.
Wong CK, Wang CB, Li ML, et al. Induction of adhesion molecules upon the interaction between eosinophils and bronchial epithelial cells: involvement of p38 MAPK and NF-kappaB. Int Immunopharmacol. 2006;6(12):1859-71.
Wong, C. K., Wang, C. B., Li, M. L., Ip, W. K., Tian, Y. P., & Lam, C. W. (2006). Induction of adhesion molecules upon the interaction between eosinophils and bronchial epithelial cells: involvement of p38 MAPK and NF-kappaB. International Immunopharmacology, 6(12), 1859-71.
Wong CK, et al. Induction of Adhesion Molecules Upon the Interaction Between Eosinophils and Bronchial Epithelial Cells: Involvement of P38 MAPK and NF-kappaB. Int Immunopharmacol. 2006 Dec 5;6(12):1859-71. PubMed PMID: 17052676.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of adhesion molecules upon the interaction between eosinophils and bronchial epithelial cells: involvement of p38 MAPK and NF-kappaB. AU - Wong,C K, AU - Wang,C B, AU - Li,M L Y, AU - Ip,W K, AU - Tian,Y P, AU - Lam,C W K, Y1 - 2006/09/01/ PY - 2006/06/16/received PY - 2006/07/17/revised PY - 2006/08/03/accepted PY - 2006/10/21/pubmed PY - 2007/1/11/medline PY - 2006/10/21/entrez SP - 1859 EP - 71 JF - International immunopharmacology JO - Int Immunopharmacol VL - 6 IS - 12 N2 - Eosinophils are principal effector cells of inflammation in allergic asthma, characterized by their infiltration and accumulation at inflammatory sites mediated by chemokine eotaxin, and interaction with adhesion molecules expressed on bronchial epithelial cells. In this study, tumor necrosis factor (TNF)-alpha and/or the interaction of eosinophils and bronchial epithelial BEAS-2B cells were found to up-regulate the cell surface expression of adhesion molecules intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 on BEAS-2B cells, and ICAM-1 and leukocyte function-associated antigen-1 (LFA-1) on eosinophils. Interaction of eosinophils and BEAS-2B cells could induce the release of granulocyte macrophage colony-stimulating factor (GM-CSF) and activate both p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB activities in BEAS-2B cells but only NF-kappaB activity in eosinophils. Both proteasome inhibitor MG-132 and selective p38 MAPK inhibitor SB 203580 could significantly decrease the expression of ICAM-1 on BEAS-2B cells and CD18 on eosinophils upon co-culture with or without TNF-alpha treatment. However, the expression of VCAM-1 on BEAS-2B cells was only up-regulated by TNF-alpha-induced NF-kappaB activity. The interaction of eosinophils and bronchial epithelial cells therefore plays an important role in the up-regulation of adhesion molecules on eosinophils and epithelial cells via differential intracellular signalling pathways during allergic inflammation. SN - 1567-5769 UR - https://www.unboundmedicine.com/medline/citation/17052676/Induction_of_adhesion_molecules_upon_the_interaction_between_eosinophils_and_bronchial_epithelial_cells:_involvement_of_p38_MAPK_and_NF_kappaB_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(06)00248-7 DB - PRIME DP - Unbound Medicine ER -