ArticlePLoS pathogens2009
Inclusion biogenesis and reactivation of persistent Chlamydia trachomatis requires host cell sphingolipid biosynthesis.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 100 citations in OpenAlex.
- High-Resolution Detection of Sphingolipids During Chlamydia trachomatis Infection via Expansion Microscopy.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Split-GFP Reporter-Based Detection of Chlamydia trachomatis Inclusion Damage.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Sphingolipids associate with the chlamydial nucleoid and mark developmental transitions in Chlamydia trachomatis.Nature communications · 2026Article
- Genetic diversity of collaborative cross mice enables the establishment of a novelInfection and immunity · 2026Article
- Ultrastructural Insights Into a Candidatus Parilichlamydia sp. Infection of Gill Goblet Cells in Greater Amberjack.Journal of fish diseases · 2025Article
- Endoplasmic reticulum: the target of chlamydial manipulation.Archives of microbiology · 2025Review
- Genome-wide identification of modulators of Chlamydia trachomatis parasitophorous vacuole stability highlights an important role for sphingolipid supply.PLoS biology · 2025Article
- Article
- Bacterial pathogens hijack host cell peroxisomes for replication vacuole expansion and integrity.Science advances · 2025Article
- Specialized contact sites regulate the fusion of chlamydial inclusion membranes.Nature communications · 2024Article
- Trifunctional sphingomyelin derivatives enable nanoscale resolution of sphingomyelin turnover in physiological and infection processes via expansion microscopy.Nature communications · 2024Article
- Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023Review
- Integrated Analysis of Gut Microbiome and Lipid Metabolism in Mice Infected with Carbapenem-ResistantMetabolites · 2022Article
- Differential Effects of Small Molecule Inhibitors on the Intracellular Chlamydia Infection.mBio · 2022Article
- Single-phagosome imaging reveals that homotypic fusion impairs phagosome degradative function.Biophysical journal · 2022Article
- Article
- A Brucella effector modulates the Arf6-Rab8a GTPase cascade to promote intravacuolar replication.The EMBO journal · 2021Article
- Akt Phosphorylation Influences Persistent Chlamydial Infection andFrontiers in cellular and infection microbiology · 2021Article
- Hijacking and Use of Host Kinases by Chlamydiae.Pathogens (Basel, Switzerland) · 2020Review
- The vacuole guard hypothesis: how intravacuolar pathogens fight to maintain the integrity of their beloved home.Current opinion in microbiology · 2020Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydiae are obligate intracellular pathogens that must coordinate the acquisition of host cell-derived biosynthetic constituents essential for bacterial survival. Purified chlamydiae contain several lipids that are typically found in eukaryotes, implying the translocation of host cell lipids to the chlamydial vacuole. Acquisition and incorporation of sphingomyelin occurs subsequent to transport from Golgi-derived exocytic vesicles, with possible intermediate transport through endosomal multivesicular bodies. Eukaryotic host cell-derived sphingomyelin is essential for intracellular growth of Chlamydia trachomatis, but the precise role of this lipid in development has not been delineated. The present study identifies specific phenotypic effects on inclusion membrane biogenesis and stability consequent to conditions of sphingomyelin deficiency. Culturing infected cells in the presence of inhibitors of serine palmitoyltransferase, the first enzyme in the biosynthetic pathway of host cell sphingomyelin, resulted in loss of inclusion membrane integrity with subsequent disruption in normal chlamydial inclusion development. Surprisingly, this was accompanied by premature redifferentiation to and release of infectious elementary bodies. Homotypic fusion of inclusions was also disrupted under conditions of sphingolipid deficiency. In addition, host cell sphingomyelin synthesis was essential for inclusion membrane stability and expansion that is vital to reactivation of persistent chlamydial infection. The present study implicates both the Golgi apparatus and multivesicular bodies as key sources of host-derived lipids, with multivesicular bodies being essential for normal inclusion development and reactivation of persistent C. trachomatis infection.
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