ArticleFrontiers in cellular and infection microbiology2013
Modulation of host immune defenses by Aeromonas and Yersinia species: convergence on toxins secreted by various secretion systems.
Article in Frontiers in cellular and infection microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
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- Cytotoxicity and Antimicrobial Resistance ofAntibiotics (Basel, Switzerland) · 2023Article
- Evaluation of Proteomic and Lipidomic Changes inInternational journal of molecular sciences · 2022Article
- In silico comparative analysis of Aeromonas Type VI Secretion System.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021Article
- Isolation of Skin Leukocytes Uncovers Phagocyte Inflammatory Responses During Induction and Resolution of Cutaneous Inflammation in Fish.Frontiers in immunology · 2021Article
- Type II Secretion Is Essential for Virulence of the Emerging Fish Pathogen, HypervirulentFrontiers in veterinary science · 2020Article
- The Outer Membrane Vesicles ofFrontiers in microbiology · 2018Article
- Comparative Genomics ofFrontiers in microbiology · 2018Article
- Yersinia pestis acetyltransferase-mediated dual acetylation at the serine and lysine residues enhances the auto-ubiquitination of ubiquitin ligase MARCH8 in human cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Piscirickettsia salmonis Imbalances the Innate Immune Response to Succeed in a Productive Infection in a Salmonid Cell Line Model.PloS one · 2016Article
- Aeromonas hydrophila virulence.Virulence · 2015Article
- Bacterial secreted effectors and caspase-3 interactions.Cellular microbiology · 2014Review
- Microbial modulation of host apoptosis and pyroptosis.Frontiers in cellular and infection microbiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Like other pathogenic bacteria, Yersinia and Aeromonas species have been continuously co-evolving with their respective hosts. Although the former is a bonafide human pathogen, the latter has gained notararity as an emerging disease-causing agent. In response to immune cell challenges, bacterial pathogens have developed diverse mechanism(s) enabling their survival, and, at times, dominance over various host immune defense systems. The bacterial type three secretion system (T3SS) is evolutionarily derived from flagellar subunits and serves as a vehicle by which microbes can directly inject/translocate anti-host factors/effector proteins into targeted host immune cells. A large number of Gram-negative bacterial pathogens possess a T3SS empowering them to disrupt host cell signaling, actin cytoskeleton re-arrangements, and even to induce host-cell apoptotic and pyroptotic pathways. All pathogenic yersiniae and most Aeromonas species possess a T3SS, but they also possess T2- and T6-secreted toxins/effector proteins. This review will focus on the mechanisms by which the T3SS effectors Yersinia outer membrane protein J (YopJ) and an Aeromonas hydrophila AexU protein, isolated from the diarrheal isolate SSU, mollify host immune system defenses. Additionally, the mechanisms that are associated with host cell apoptosis/pyroptosis by Aeromonas T2SS secreted Act, a cytotoxic enterotoxin, and Hemolysin co-regulated protein (Hcp), an A. hydrophila T6SS effector, will also be discussed.
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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.