ReviewImmunologic research2004
Bacterial inhibition of eukaryotic pro-inflammatory pathways.
Review in Immunologic research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Highlighting the Relevance of Gut Microbiota Manipulation in Inflammatory Bowel Disease.Diagnostics (Basel, Switzerland) · 2021Review
- PROBIOTIC APPROACHES FOR TARGETING INFLAMMATORY BOWEL DISEASE: AN UPDATE ON ADVANCES AND OPPORTUNITIES IN MANAGING THE DISEASE.International journal of probiotics & prebiotics · 2016Article
- Improvement in Th1/Th2 immune homeostasis, antioxidative status and resistance to pathogenic E. coli on consumption of probiotic Lactobacillus rhamnosus fermented milk in aging mice.Age (Dordrecht, Netherlands) · 2014Article
- A Yersinia effector with enhanced inhibitory activity on the NF-κB pathway activates the NLRP3/ASC/caspase-1 inflammasome in macrophages.PLoS pathogens · 2011Article
- Epigenome targeting by probiotic metabolites.Gut pathogens · 2010Article
- Enteropathogenic E. coli non-LEE encoded effectors NleH1 and NleH2 attenuate NF-κB activation.Molecular microbiology · 2010Article
- Necrotizing enterocolitis: a multifactorial disease with no cure.World journal of gastroenterology · 2008Review
- Modulation of the NF-kappaB pathway by Bordetella pertussis filamentous hemagglutinin.PloS one · 2008Article
- Probiotics and inflammatory bowel diseases.Postgraduate medical journal · 2006Review
- Animal models of intestinal inflammation: ineffective communication between coalition members.Springer seminars in immunopathology · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic cells perceive and respond to microbes, both pathogenic and commensal, by activation of signaling cascades such as the NF-kappaB pathway. Induction of such pathways leads to the upregulation of a program of gene expression that mediates pro-inflammatory and anti-apoptotic effector proteins. This host response is usually effective in clearing or controlling an infection. For pathogens (and potentially, symbionts) to continue their lifecycle, it is necessary to evade or repress these cellular responses. There has been recent interest in bacteria that can inhibit pro-inflammatory pathways, in some cases by the actions of soluble effector proteins secreted via a Type III secretion system. Certain effector proteins with this function possess enzymatic activity toward ubiquitin and related molecules. Ubiquitination is an increasingly recognized regulatory modification in eukaryotic cells, and microbial effectors that modulate this key host system may have diverse effects on infected cells and mediate many aspects of eukaryotic-prokaryotic interactions.
Indexed as
Identifiers
15181280What OpenQuestion holds
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.