ArticleBMC biology2018
Phthiocerol dimycocerosates promote access to the cytosol and intracellular burden of Mycobacterium tuberculosis in lymphatic endothelial cells.
Article in BMC biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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52 citing papers in PubMed, 118 citations in OpenAlex.
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- Development of force field parameters for the atomic simulation of Mycobacterial membranes.Communications chemistry · 2025Article
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- Real-time visualization reveals Mycobacterium tuberculosis ESAT-6 disrupts phagosome-like compartment via fibril-mediated vesiculation.Cell reports · 2025Article
- Context matters: assessing the impacts of genomic background and ecology on microbial biosynthetic gene cluster evolution.mSystems · 2025Review
- Mycobacterium tuberculosis virulence lipid PDIM inhibits autophagy in mice.Nature microbiology · 2024Article
- Mycobacterial CpsA activates type I IFN signaling in macrophages via cGAS-mediated pathway.iScience · 2024Article
- Temporal genome-wide fitness analysis ofmSystems · 2024Article
- Intricate link between siderophore secretion and drug efflux inAntimicrobial agents and chemotherapy · 2023Article
- High content quantitative imaging of Mycobacterium tuberculosis responses to acidic microenvironments within human macrophages.FEBS open bio · 2023Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPhthiocerol dimycocerosates (PDIM), glycolipids found on the outer surface of virulent members of the Mycobacterium tuberculosis (Mtb) complex, are a major contributing factor to the pathogenesis of Mtb. Myelocytic cells, such as macrophages and dendritic cells, are the primary hosts for Mtb after infection and previous studies have shown multiple roles for PDIM in supporting Mtb in these cells. However, Mtb can infect other cell types. We previously showed that Mtb efficiently replicates in human lymphatic endothelial cells (hLECs) and that the hLEC cytosol acts as a reservoir for Mtb in humans. Here, we examined the role of PDIM in Mtb translocation to the cytosol in hLECs.
resultsAnalysis of a Mtb mutant unable to produce PDIM showed less co-localisation of bacteria with the membrane damage marker Galectin-8 (Gal8), indicating that PDIM strongly contribute to phagosomal membrane damage. Lack of this Mtb lipid also leads to a reduction in the proportion of Mtb co-localising with markers of macroautophagic removal of intracellular bacteria (xenophagy) such as ubiquitin, p62 and NDP52. hLEC imaging with transmission electron microscopy shows that Mtb mutants lacking PDIM are much less frequently localised in the cytosol, leading to a lower intracellular burden.
conclusionsPDIM is needed for the disruption of the phagosome membrane in hLEC, helping Mtb avoid the hydrolytic phagolysosomal milieu. It facilitates the translocation of Mtb into the cytosol, and the decreased intracellular burden of Mtb lacking PDIM indicates that the cytosol is the preferred replicative niche for Mtb in these cells. We hypothesise that pharmacological targeting of PDIM synthesis in Mtb would reduce the formation of a lymphatic reservoir of Mtb in humans.
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