ArticleInfection and immunity2012
The Mycobacterium tuberculosis SecA2 system subverts phagosome maturation to promote growth in macrophages.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed.
- Cycloserine inhibits glutamate decarboxylase fromJournal of enzyme inhibition and medicinal chemistry · 2026Article
- Sorting nexin 5 deficiency impairs MHC class II antigen presentation and inflammatory responses during tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Mitochondrial STAT3-mediated suppression of apoptosis constrains antimycobacterial immunity.bioRxiv : the preprint server for biology · 2026Article
- Sorting nexin 5 mediates antigen presentation and immunity againstbioRxiv : the preprint server for biology · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- A Study to Asses Effects of Diabetes Mellitus on Treatment Outcome of Tuberculosis Patients.Journal of pharmacy & bioallied sciences · 2025Article
- Development and preclinical evaluation of next-generation ΔsigH-based live candidate vaccines.JCI insight · 2025Article
- Review
- Research progress on protein tyrosine phosphatase A from Mycobacterium tuberculosis.Frontiers in immunology · 2025Review
- The SapM phosphatase can arrest phagosome maturation in an ESX-1 independent manner inInfection and immunity · 2024Article
- Article
- Mycobacterium tuberculosis SecA2-dependent activation of host Rig-I/MAVs signaling is not conserved in Mycobacterium marinum.PloS one · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- Mycobacterium tuberculosis and its clever approaches to escape the deadly macrophage.World journal of microbiology & biotechnology · 2023Review
- Virulence Factors ofPathogens (Basel, Switzerland) · 2023Review
- Pathogenicity of Type I Interferons inInternational journal of molecular sciences · 2023Review
- Mycobacterium smegmatis: The Vanguard of Mycobacterial Research.Journal of bacteriology · 2023Review
- Mechanisms of lung damage in tuberculosis: implications for chronic obstructive pulmonary disease.Frontiers in cellular and infection microbiology · 2023Review
- Characteristics ofFrontiers in cellular and infection microbiology · 2023Article
- Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The ability of Mycobacterium tuberculosis to grow in macrophages is critical to the virulence of this important pathogen. One way M. tuberculosis is thought to maintain a hospitable niche in macrophages is by arresting the normal process of phagosomes maturing into acidified phagolysosomes. The process of phagosome maturation arrest by M. tuberculosis is not fully understood, and there has remained a need to firmly establish a requirement for phagosome maturation arrest for M. tuberculosis growth in macrophages. Other intracellular pathogens that control the phagosomal environment use specialized protein export systems to deliver effectors of phagosome trafficking to the host cell. In M. tuberculosis, the accessory SecA2 system is a specialized protein export system that is required for intracellular growth in macrophages. In studying the importance of the SecA2 system in macrophages, we discovered that SecA2 is required for phagosome maturation arrest. Shortly after infection, phagosomes containing a ΔsecA2 mutant of M. tuberculosis were more acidified and showed greater association with markers of late endosomes than phagosomes containing wild-type M. tuberculosis. We further showed that inhibitors of phagosome acidification rescued the intracellular growth defect of the ΔsecA2 mutant, which demonstrated that the phagosome maturation arrest defect of the ΔsecA2 mutant is responsible for the intracellular growth defect. This study demonstrates the importance of phagosome maturation arrest for M. tuberculosis growth in macrophages, and it suggests there are effectors of phagosome maturation that are exported into the host environment by the accessory SecA2 system.
Indexed as
Identifiers
What 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.