PMID- 23250951
OWN - NLM
STAT- MEDLINE
DCOM- 20130418
LR  - 20211021
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 81
IP  - 3
DP  - 2013 Mar
TI  - 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.
PG  - 673-83
LID - 10.1128/IAI.01043-12 [doi]
AB  - 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 1alpha 
      (MIP-1alpha), MIP-1beta, and granulocyte colony-stimulating factor (G-CSF) also 
      significantly increased in U937 cells. ArtB also upregulated the cytokines tumor 
      necrosis factor alpha (TNF-alpha) 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.
FAU - Wang, Hui
AU  - Wang H
AD  - Research Centre for Infectious Diseases, School of Molecular and Biomedical 
      Science, University of Adelaide, South Australia, Australia.
FAU - Paton, James C
AU  - Paton JC
FAU - Herdman, Brock P
AU  - Herdman BP
FAU - Rogers, Trisha J
AU  - Rogers TJ
FAU - Beddoe, Travis
AU  - Beddoe T
FAU - Paton, Adrienne W
AU  - Paton AW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121217
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Bacterial Toxins)
RN  - 0 (Cytokines)
RN  - 0 (Protein Subunits)
SB  - IM
MH  - Bacterial Toxins/chemistry/*toxicity
MH  - Brain/blood supply
MH  - Cell Adhesion/physiology
MH  - Cell Line
MH  - Cytokines/genetics/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/*drug effects/metabolism
MH  - Epithelial Cells/*drug effects/metabolism
MH  - Gene Expression Regulation/drug effects/immunology
MH  - Humans
MH  - Intestinal Mucosa/cytology
MH  - Macrophages/*drug effects/metabolism
MH  - Protein Subunits/chemistry/metabolism
MH  - Salmonella typhi/*metabolism
PMC - PMC3584882
EDAT- 2012/12/20 06:00
MHDA- 2013/04/20 06:00
PMCR- 2013/09/01
CRDT- 2012/12/20 06:00
PHST- 2012/12/20 06:00 [entrez]
PHST- 2012/12/20 06:00 [pubmed]
PHST- 2013/04/20 06:00 [medline]
PHST- 2013/09/01 00:00 [pmc-release]
AID - IAI.01043-12 [pii]
AID - 01043-12 [pii]
AID - 10.1128/IAI.01043-12 [doi]
PST - ppublish
SO  - Infect Immun. 2013 Mar;81(3):673-83. doi: 10.1128/IAI.01043-12. Epub 2012 Dec 17.