ArticleBritish journal of pharmacology2003
Verotoxin activates mitogen-activated protein kinase in human peripheral blood monocytes: role in apoptosis and proinflammatory cytokine release.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 42 citations in OpenAlex.
- Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli.Cellular and molecular neurobiology · 2023Article
- Shiga Toxins as Antitumor Tools.Toxins · 2021Review
- Therapeutic Uses of Bacterial Subunit Toxins.Toxins · 2021Review
- Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli.PLoS pathogens · 2021Article
- The Role ofToxins · 2020Review
- Molecular Biology ofToxins · 2020Review
- Rescue from Stx2-Producing E. coli-Associated Encephalopathy by Intravenous Injection of Muse Cells in NOD-SCID Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Activation of the Classical Mitogen-Activated Protein Kinases Is Part of the Shiga Toxin-Induced Ribotoxic Stress Response and May Contribute to Shiga Toxin-Induced Inflammation.Infection and immunity · 2016Article
- Effect of shiga toxin and its subunits on cytokine induction in different cell lines.International journal of molecular and cellular medicine · 2014Article
- Shiga toxins expressed by human pathogenic bacteria induce immune responses in host cells.Journal of microbiology (Seoul, Korea) · 2013Review
- Regulation of cytokine and chemokine expression by the ribotoxic stress response elicited by Shiga toxin type 1 in human macrophage-like THP-1 cells.Infection and immunity · 2012Article
- Activation of cell stress response pathways by Shiga toxins.Cellular microbiology · 2012Review
- Article
- Over-expression of mitogen-activated protein kinase phosphatase-2 enhances adhesion molecule expression and protects against apoptosis in human endothelial cells.British journal of pharmacology · 2010Article
- Shiga toxins: intracellular trafficking to the ER leading to activation of host cell stress responses.Toxins · 2010Review
- Global transcriptional response of macrophage-like THP-1 cells to Shiga toxin type 1.Infection and immunity · 2010Article
- Shiga toxins--from cell biology to biomedical applications.Nature reviews. Microbiology · 2010Review
- Shiga toxin 1-induced proinflammatory cytokine production is regulated by the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin signaling pathway.Infection and immunity · 2009Article
- p38 mitogen-activated protein kinase mediates lipopolysaccharide and tumor necrosis factor alpha induction of shiga toxin 2 sensitivity in human umbilical vein endothelial cells.Infection and immunity · 2008Article
- The Mitogen-activated protein kinase p38 links Shiga Toxin-dependent signaling and trafficking.Molecular biology of the cell · 2008Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
. In this study, we examined the role of mitogen-activated protein (MAP) kinases in the effects of verotoxins (VTs), from Escherichia coli O157:H7, upon both apoptosis and the release of tumour necrosis factor alpha (TNF-alpha) and granulocyte-macrophage colony-stimulated factor (GM-CSF) from human monocytes. 2. Both VT1 and VT2 stimulated a weak, transient increase in c-Jun-N-terminal kinase (JNK) activity and a strong activation of both p38 mitogen-activated protein kinase (MAP kinase) and extracellular-regulated kinase (ERK) activity in human monocytes, which was sustained in the case of p38 MAP kinase. 3. Stimulation of human monocytes with VT2 (100 ng ml-1) did not result in an increase in apoptosis; however, the toxin stimulated the release of both TNF-alpha and GM-CSF. 4. Pretreatment of human monocytes with the p38 MAP kinase inhibitor SB203580, at concentrations from 100 nM to 10 microM, significantly decreased the VT1- and VT2-induced TNF-alpha and GM-CSF release from monocytes. In contrast, inhibition of MEK1 with PD98059 only significantly decreased GM-CSF release. 5. Pretreatment of monocytes with SP600125 inhibited both GM-CSF and TNF-alpha production; however, significant effects upon p38 MAP kinase and ERK activation were observed. 6. Taken together, these results suggest a role for p38 MAP kinase and ERK in cytokine generation in response to the verotoxins. A role for JNK remains undetermined.
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