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Expression of cytokine, chemokine, and adhesion molecules during endothelial cell activation induced by antibodies against dengue virus nonstructural protein 1.
J Immunol. 2005 Jan 01; 174(1):395-403.JI

Abstract

Vascular dysfunction is a hallmark associated with disease onset in dengue hemorrhagic fever and dengue shock syndrome. In addition to direct viral damage, immune responses to dengue virus (DV) infection may also underlie the pathogenesis of disease. We have proposed a mechanism of molecular mimicry in which Abs directed against DV nonstructural protein 1 (NS1) cross-react with endothelial cells and induce damage. In this study, we demonstrated the inflammatory endothelial cell activation induced by anti-DV NS1 via the transcription factor NF-kappaB-regulated pathway. Protein phosphorylation and NF-kappaB activation were observed after anti-DV NS1 stimulation in a human microvascular endothelial cell line-1. The cytokine and chemokine production, including IL-6, IL-8, and MCP-1, but not RANTES, in endothelial cells increased after treatment with anti-DV NS1 Abs. The expression of IL-6, IL-8, and MCP-1 was blocked by the preabsorption of anti-DV NS1 with DV NS1 or by the inhibition of NF-kappaB activation. Furthermore, the increases in both ICAM-1 expression and the ability of human PBMC to adhere to endothelial cells were also observed, and these effects were inhibited by pretreatment with anti-ICAM-1 or anti-MCP-1 Abs. Therefore, in addition to endothelial cell apoptosis, as previously reported, inflammatory activation occurs in endothelial cells after stimulation by anti-DV NS1 Abs. These results suggest the involvement of anti-DV NS1 Abs in the vasculopathy of DV infection.

Authors+Show Affiliations

Department of Micribiology and Immunology, National Cheng Kung University Medical College, 1 University Road, Tainan 701, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

15611263

Citation

Lin, Chiou-Feng, et al. "Expression of Cytokine, Chemokine, and Adhesion Molecules During Endothelial Cell Activation Induced By Antibodies Against Dengue Virus Nonstructural Protein 1." Journal of Immunology (Baltimore, Md. : 1950), vol. 174, no. 1, 2005, pp. 395-403.
Lin CF, Chiu SC, Hsiao YL, et al. Expression of cytokine, chemokine, and adhesion molecules during endothelial cell activation induced by antibodies against dengue virus nonstructural protein 1. J Immunol. 2005;174(1):395-403.
Lin, C. F., Chiu, S. C., Hsiao, Y. L., Wan, S. W., Lei, H. Y., Shiau, A. L., Liu, H. S., Yeh, T. M., Chen, S. H., Liu, C. C., & Lin, Y. S. (2005). Expression of cytokine, chemokine, and adhesion molecules during endothelial cell activation induced by antibodies against dengue virus nonstructural protein 1. Journal of Immunology (Baltimore, Md. : 1950), 174(1), 395-403.
Lin CF, et al. Expression of Cytokine, Chemokine, and Adhesion Molecules During Endothelial Cell Activation Induced By Antibodies Against Dengue Virus Nonstructural Protein 1. J Immunol. 2005 Jan 1;174(1):395-403. PubMed PMID: 15611263.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of cytokine, chemokine, and adhesion molecules during endothelial cell activation induced by antibodies against dengue virus nonstructural protein 1. AU - Lin,Chiou-Feng, AU - Chiu,Shu-Chen, AU - Hsiao,Yu-Ling, AU - Wan,Shu-Wen, AU - Lei,Huan-Yao, AU - Shiau,Ai-Li, AU - Liu,Hsiao-Sheng, AU - Yeh,Trai-Ming, AU - Chen,Shun-Hua, AU - Liu,Ching-Chuan, AU - Lin,Yee-Shin, PY - 2004/12/22/pubmed PY - 2005/1/28/medline PY - 2004/12/22/entrez SP - 395 EP - 403 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 174 IS - 1 N2 - Vascular dysfunction is a hallmark associated with disease onset in dengue hemorrhagic fever and dengue shock syndrome. In addition to direct viral damage, immune responses to dengue virus (DV) infection may also underlie the pathogenesis of disease. We have proposed a mechanism of molecular mimicry in which Abs directed against DV nonstructural protein 1 (NS1) cross-react with endothelial cells and induce damage. In this study, we demonstrated the inflammatory endothelial cell activation induced by anti-DV NS1 via the transcription factor NF-kappaB-regulated pathway. Protein phosphorylation and NF-kappaB activation were observed after anti-DV NS1 stimulation in a human microvascular endothelial cell line-1. The cytokine and chemokine production, including IL-6, IL-8, and MCP-1, but not RANTES, in endothelial cells increased after treatment with anti-DV NS1 Abs. The expression of IL-6, IL-8, and MCP-1 was blocked by the preabsorption of anti-DV NS1 with DV NS1 or by the inhibition of NF-kappaB activation. Furthermore, the increases in both ICAM-1 expression and the ability of human PBMC to adhere to endothelial cells were also observed, and these effects were inhibited by pretreatment with anti-ICAM-1 or anti-MCP-1 Abs. Therefore, in addition to endothelial cell apoptosis, as previously reported, inflammatory activation occurs in endothelial cells after stimulation by anti-DV NS1 Abs. These results suggest the involvement of anti-DV NS1 Abs in the vasculopathy of DV infection. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/15611263/Expression_of_cytokine_chemokine_and_adhesion_molecules_during_endothelial_cell_activation_induced_by_antibodies_against_dengue_virus_nonstructural_protein_1_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=15611263 DB - PRIME DP - Unbound Medicine ER -