ArticlePloS one2011
The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.
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Who cites it
112 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.
- Guideline
- SmartVax-Bp: An Immunoinformatic guided Multi-Epitope Vaccine Blueprint Against Burkholderia pseudomallei.Probiotics and antimicrobial proteins · 2026Article
- Systematic discovery of novel phosphoinositide-binding effectors inMicrobiology spectrum · 2026Article
- Secretion systems shaping host-pathogen interactions in Burkholderia species.Applied microbiology and biotechnology · 2026Review
- Trigger Factor inJournal of bacteriology · 2026Article
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- Hijacking the Ubl code: bacterial manipulation of ubiquitin-like proteins.Essays in biochemistry · 2025Review
- Systematic Discovery of Novel Phosphoinositide-Binding Effectors inbioRxiv : the preprint server for biology · 2025Article
- The battle between bacterial infection and autophagy in aquatic animals.Frontiers in immunology · 2025Review
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Genomic dataset of eighteenCurrent research in microbial sciences · 2025Article
- Performance of Antibody-Detection Tests for Human Melioidosis: A Systematic Review and Meta-analysis.The Malaysian journal of medical sciences : MJMS · 2024Review
- Article
- Bacterial esterases reverse lipopolysaccharide ubiquitylation to block host immunity.Cell host & microbe · 2024Article
- Burkholderia pseudomallei BipD modulates host mitophagy to evade killing.Nature communications · 2024Article
- TetR-like regulator BP1026B_II1561 controls aromatic amino acid biosynthesis and intracellular pathogenesis inFrontiers in microbiology · 2024Article
- Inhibition of macrophage infectivity potentiator inFrontiers in cellular and infection microbiology · 2024Article
- Risk Factors for Melioidosis Mortality and Epidemics: A Multicentre, 10-Year Retrospective Cohort Study in Northern Hainan.Infectious diseases and therapy · 2023Article
- DRAM1 confers resistance toAutophagy reports · 2023Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Burkholderia pseudomallei is the causative agent of melioidosis, a fatal infectious disease endemic in tropical regions worldwide, and especially prevalent in southeast Asia and northern Australia. This intracellular pathogen can escape from phagosomes into the host cytoplasm, where it replicates and infects adjacent cells. We previously demonstrated that, in response to B. pseudomallei infection of macrophage cell line RAW 264.7, a subset of bacteria co-localized with the autophagy marker protein, microtubule-associated protein light chain 3 (LC3), implicating autophagy in host cell defence against infection. Recent reports have suggested that LC3 can be recruited to both phagosomes and autophagosomes, thereby raising questions regarding the identity of the LC3-positive compartments in which invading bacteria reside and the mechanism of the autophagic response to B. pseudomallei infection. Electron microscopy analysis of infected cells demonstrated that the invading bacteria were either free in the cytosol, or sequestered in single-membrane phagosomes rather than double-membrane autophagosomes, suggesting that LC3 is recruited to B. pseudomallei-containing phagosomes. Partial or complete loss of function of type III secretion system cluster 3 (TTSS3) in mutants lacking the BopA (effector) or BipD (translocator) proteins respectively, resulted in delayed or no escape from phagosomes. Consistent with these observations, bopA and bipD mutants both showed a higher level of co-localization with LC3 and the lysosomal marker LAMP1, and impaired survival in RAW264.7 cells, suggesting enhanced killing in phagolysosomes. We conclude that LC3 recruitment to phagosomes stimulates killing of B. pseudomallei trapped in phagosomes. Furthermore, BopA plays an important role in efficient escape of B. pseudomallei from phagosomes.
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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.