ArticleInfection and immunity2008
Macrophage migration inhibitory factor and interleukin-8 produced by gastric epithelial cells during Helicobacter pylori exposure induce expression and activation of the epidermal growth factor receptor.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Tyrosine Kinases inToxins · 2019Review
- Correlation between macrophage migration inhibitory factor and autophagy in Helicobacter pylori-associated gastric carcinogenesis.PloS one · 2019Article
- Silent Witness: Dual-Species Transcriptomics Reveals Epithelial Immunological Quiescence to Helminth Larval Encounter and Fostered Larval Development.Frontiers in immunology · 2018Article
- Expression of cluster of differentiation 74 in gallbladder carcinoma and the correlation with epithelial growth factor receptor levels.Oncology letters · 2016Article
- A specific A/T polymorphism in Western tyrosine phosphorylation B-motifs regulates Helicobacter pylori CagA epithelial cell interactions.PLoS pathogens · 2015Article
- Toll-like receptors expression in follicular cells of patients with poor ovarian response.International journal of fertility & sterility · 2014Article
- Trichomonas vaginalis homolog of macrophage migration inhibitory factor induces prostate cell growth, invasiveness, and inflammatory responses.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Increased ERK signalling promotes inflammatory signalling in primary airway epithelial cells expressing Z α1-antitrypsin.Human molecular genetics · 2014Article
- Article
- Enterococcus faecalis enhances cell proliferation through hydrogen peroxide-mediated epidermal growth factor receptor activation.Infection and immunity · 2012Article
- CD74 and macrophage migration inhibitory factor as therapeutic targets in gastric cancer.World journal of gastroenterology · 2012Article
- Enhanced expression of CD74 in gastrointestinal cancers and benign tissues.International journal of clinical and experimental pathology · 2010Article
- Review
- Association of LEC and tnpA Helicobacter pylori genes with gastric cancer in a Brazilian population.Infectious agents and cancer · 2010Article
- CD74 in antigen presentation, inflammation, and cancers of the gastrointestinal tract.World journal of gastroenterology · 2009Review
- Detailed Investigation of Downstream TLR Signaling in the Follicular Cells of Women with Endometriosis.Journal of reproduction & infertilityArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
While a link between Helicobacter pylori exposure and gastric cancer has been established, the underlying mechanisms remain unclear. H. pylori induces a chronic inflammatory response in infected individuals. A link between chronic inflammation and carcinogenesis has long been suggested but never elucidated. Epidermal growth factor receptor (EGFR) signaling plays an important role in both proinflammatory and procarcinogenic mechanisms and is upregulated on gastric epithelial cells (GECs) during H. pylori exposure. The aim of this study was to examine the effects of two important proinflammatory cytokines released during H. pylori infection, macrophage migration inhibitory factor (MIF) and interleukin-8 (IL-8), on the expression and transactivation of EGFR and on the proliferation of GECs during H. pylori exposure. The expression of EGFR by GECs was increased by exposure to either H. pylori, recombinant MIF, or recombinant IL-8. However, cag pathogenicity island knockout strains of H. pylori had very little effect on expression. MIF and IL-8 also induced phosphorylation of EGFR, signaling events, and proliferation during H. pylori exposure, all of which were decreased when they were neutralized by these cytokines or were blocked from their receptors. The overall role of EGFR in these responses to H. pylori exposure was assessed by knocking down EGFR expression by small interfering RNA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.