ArticlePLoS pathogens2017
Systematic, multiparametric analysis of Mycobacterium tuberculosis intracellular infection offers insight into coordinated virulence.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 123 citations in OpenAlex.
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- The lipid language of tuberculosis:mBio · 2026Review
- PDIM/PGL-deficientMicrobiology resource announcements · 2026Article
- Isolation, identification and genomic analysis of Mycobacterium caprae strain SY-1 from Chinese sika deer (Cervus nippon).BMC genomics · 2026Article
- Circulating antibody signatures againstFrontiers in immunology · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Protein kinase F regulates the virulence ofbioRxiv : the preprint server for biology · 2025Article
- Mycobacterium tuberculosis biology, pathogenicity and interaction with the host.Nature reviews. Microbiology · 2025Review
- Control of antigen presentation on MHC-I by a bacterial secretion system.bioRxiv : the preprint server for biology · 2025Article
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- Targeting infection-specific peptides in immunopeptidomics studies for vaccine target discovery.The Journal of experimental medicine · 2025Article
- Mycobacterial phthiocerol dimycocerosate induces Galectin-3 upregulation to impair proinflammatory responses and favor immune evasion.International journal of biological macromolecules · 2025Article
- NProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unraveling Mycobacterium tuberculosis acid resistance and pH homeostasis mechanisms.FEBS letters · 2025Review
- Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
A key to the pathogenic success of Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, is the capacity to survive within host macrophages. Although several factors required for this survival have been identified, a comprehensive knowledge of such factors and how they work together to manipulate the host environment to benefit bacterial survival are not well understood. To systematically identify Mtb factors required for intracellular growth, we screened an arrayed, non-redundant Mtb transposon mutant library by high-content imaging to characterize the mutant-macrophage interaction. Based on a combination of imaging features, we identified mutants impaired for intracellular survival. We then characterized the phenotype of infection with each mutant by profiling the induced macrophage cytokine response. Taking a systems-level approach to understanding the biology of identified mutants, we performed a multiparametric analysis combining pathogen and host phenotypes to predict functional relationships between mutants based on clustering. Strikingly, mutants defective in two well-known virulence factors, the ESX-1 protein secretion system and the virulence lipid phthiocerol dimycocerosate (PDIM), clustered together. Building upon the shared phenotype of loss of the macrophage type I interferon (IFN) response to infection, we found that PDIM production and export are required for coordinated secretion of ESX-1-substrates, for phagosomal permeabilization, and for downstream induction of the type I IFN response. Multiparametric clustering also identified two novel genes that are required for PDIM production and induction of the type I IFN response. Thus, multiparametric analysis combining host and pathogen infection phenotypes can be used to identify novel functional relationships between genes that play a role in infection.
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Registered trials
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