ArticleMicrobial pathogenesis2009
Inhibition of heat shock protein expression by Helicobacter pylori.
Article in Microbial pathogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- The microbiota-proteostasis axis: implications in neurodegenerative diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Live Attenuated Measles Virus Vaccine ExpressingMolecular therapy oncolytics · 2020Article
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- Molecular and Physiological Study ofProteomes · 2018Review
- The Interplay between Two Transcriptional Repressors and Chaperones OrchestratesInternational journal of molecular sciences · 2018Review
- The Helicobacter pylori cytotoxin CagA is essential for suppressing host heat shock protein expression.Cell stress & chaperones · 2016Article
- Description of the interaction between Candida albicans and macrophages by mixed and quantitative proteome analysis without isolation.AMB Express · 2015Article
- H. pylori infection, inflammation and gastric cancer.Journal of gastrointestinal cancer · 2014Review
- Comparative proteomics analysis of sarcosine insoluble outer membrane proteins from clarithromycin resistant and sensitive strains of Helicobacter pylori.Journal of microbiology (Seoul, Korea) · 2013Article
- Heat shock protein 70 (HSP70) expression is associated with poor prognosis in intestinal type gastric cancer.Virchows Archiv : an international journal of pathology · 2013Article
- Host cell responses to persistent mycoplasmas--different stages in infection of HeLa cells with Mycoplasma hominis.PloS one · 2013Article
- Down-regulation of HSP70 sensitizes gastric epithelial cells to apoptosis and growth retardation triggered by H. pylori.BMC gastroenterology · 2011Article
- Pseudomonas syringae hijacks plant stress chaperone machinery for virulence.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Role of innate immunity in Helicobacter pylori-induced gastric malignancy.Physiological reviews · 2010Review
- Surreptitious manipulation of the human host by Helicobacter pylori.Gut microbes · 2010Article
- Heat shock protein: hard worker or bad offender for gastric diseases.International journal of proteomics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Heat shock proteins (HSPs) are primarily known as molecular chaperones that are induced by cell stress and prevent protein aggregation and facilitate folding. Recent evidence suggests that exposure of cells to microbial pathogens can also induce HSPs, which then modulate both innate and adaptive immune responses. Paradoxically, Helicobacter pylori has been found to decrease expression of HSPs. We sought to investigate this phenomenon further and to examine the role of different H. pylori strains and recognized virulence factors in cell culture and in the mouse model. Co-culture of H. pylori with two gastric carcinoma cell lines reduced expression of HSP70 and, to a lesser extent, HSP60. Down modulation of HSPs was not dependent on the presence of the vacuolating cytotoxin (VacA) or the cag pathogenicity island (cag PAI). C57BL/6 mice infected with a human H. pylori strain also demonstrated reduced expression of HSP70, HSP8, and heat shock factor 1 (HSF-1), a transcriptional activator of HSP70. In contrast, the bacterial pathogen, S. Typhimurium up-regulated HSP expression. Since HSPs are thought to function as danger signals during microbial infection, H. pylori down-regulation of HSPs may be a mechanism of immune evasion that promotes chronic infection.
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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.