ArticleBMC microbiology2014
Type three secretion system-mediated escape of Burkholderia pseudomallei into the host cytosol is critical for the activation of NFκB.
Article in BMC microbiology, 2014. 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
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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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Secretion systems shaping host-pathogen interactions in Burkholderia species.Applied microbiology and biotechnology · 2026Review
- Article
- Article
- Melioidosis.Nature reviews. Disease primers · 2018Review
- Review
- Immune Recognition of the Epidemic Cystic Fibrosis Pathogen Burkholderia dolosa.Infection and immunity · 2017Article
- Type III Secretion in the Melioidosis PathogenFrontiers in cellular and infection microbiology · 2017Review
- Modifying the Mitochondrial Genome.Cell metabolism · 2016Review
- Characterization and analysis of the Burkholderia pseudomallei BsaN virulence regulon.BMC microbiology · 2014Article
- Dual RNA-seq reveals a type 6 secretion system-dependent blockage of TNF-α signaling and BicA as aGut microbesArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundBurkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease endemic in Southeast Asia and Northern Australia. This Gram-negative pathogen possesses numerous virulence factors including three "injection type" type three secretion systems (T3SSs). B. pseudomallei has been shown to activate NFκB in HEK293T cells in a Toll-like receptor and MyD88 independent manner that requires T3SS gene cluster 3 (T3SS3 or T3SSBsa). However, the mechanism of how T3SS3 contributes to NFκB activation is unknown.
resultsKnown T3SS3 effectors are not responsible for NFκB activation. Furthermore, T3SS3-null mutants are able to activate NFκB almost to the same extent as wildtype bacteria at late time points of infection, corresponding to delayed escape into the cytosol. NFκB activation also occurs when bacteria are delivered directly into the cytosol by photothermal nanoblade injection.
conclusionsT3SS3 does not directly activate NFκB but facilitates bacterial escape into the cytosol where the host is able to sense the presence of the pathogen through cytosolic sensors leading to NFκB activation.
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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.