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|Title:||The b subunit of an AB5 toxin produced by salmonella enterica serovar typhi up-regulates chemokines, cytokines, and adhesion molecules in human macrophage, colonic epithelial, and brain microvascular endothelial cell lines|
|Citation:||Infection and Immunity, 2013; 81(3):673-683|
|Publisher:||Amer Soc Microbiology|
|Hui Wang, James C. Paton, Brock P. Herdman, Trisha J. Rogers, Travis Beddoe, Adrienne W. Paton|
|Abstract:||The principal function of bacterial AB5 toxin B subunits is to interact with glycan receptors on the surfaces of target cells and mediate the internalization of holotoxin. However, B subunit-receptor interactions also have the potential to impact cell signaling pathways and, in so doing, contribute to pathogenesis independently of the catalytic (toxic) A subunits. Various Salmonella enterica serovars, including Salmonella enterica serovar Typhi, encode an AB5 toxin (ArtAB), the A subunit of which is an ADP-ribosyltransferase related to the S1 subunit of pertussis toxin. However, although the A subunit is able to catalyze ADP-ribosylation of host G proteins, a cytotoxic phenotype has yet to be identified for the holotoxin. We therefore examined the capacity of the purified B subunit (ArtB) from S. Typhi to elicit cytokine, chemokine, and adhesion molecule responses in human macrophage (U937), colonic epithelial (HCT-8) cell, and brain microvascular endothelial cell (HBMEC) lines. Secretion of the chemokines monocyte chemotactic protein 1 (MCP-1) and interleukin 8 (IL-8) was increased in all three tested cell lines, with macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and granulocyte colony-stimulating factor (G-CSF) also significantly increased in U937 cells. ArtB also upregulated the cytokines tumor necrosis factor alpha (TNF-α) and IL-6 in HBMECs and HCT-8 cells, but not in U937 cells, while intercellular adhesion molecule 1 (ICAM-1) was upregulated in HCT-8 and U937 cells and vascular cell adhesion molecule 1 (VCAM-1) was upregulated in HBMECs. Thus, ArtB may contribute to pathogenesis independently of the A subunit by promoting and maintaining a strong inflammatory response at the site of infection.|
|Keywords:||Intestinal Mucosa; Brain; Cell Line; Macrophages; Endothelial Cells; Epithelial Cells; Humans; Salmonella typhi; Protein Subunits; Bacterial Toxins; Cytokines; Cell Adhesion; Gene Expression Regulation; Dose-Response Relationship, Drug|
|Rights:||Copyright © 2013, American Society for Microbiology. All Rights Reserved.|
|Appears in Collections:||Molecular and Biomedical Science publications|
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