Lipid droplet dynamics at early stages of Mycobacterium marinum infection in Dictyostelium. (8th April 2015)

• Record Type: Journal Article
• Authors: Barisch, Caroline; Paschke, Peggy; Hagedorn, Monica; Maniak, Markus; Soldati, Thierry
• Is Part Of: Cellular microbiology. Volume 17:Number 9(2015:Sep.)
• Page Start: 1332
• Page End: 1349
• Publication Date: 2015-04-08
• Subjects: Microbiology -- Periodicals; Cytology -- Periodicals; Host-parasite relationships -- Periodicals; Microbiology -- Periodicals; Cells -- Periodicals; Microbiologie -- Périodiques; Microbiologie; Relation hôte-parasite; Cytologie; Cellule; Réponse cellulaire; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); 579.05
• DOI: 10.1111/cmi.12437
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>Lipid droplets exist in virtually every cell type, ranging not only from mammals to plants, but also to eukaryotic and prokaryotic unicellular organisms such as <italic>D</italic><italic>ictyostelium</italic> and bacteria. They serve among other roles as energy reservoir that cells consume in times of starvation. Mycobacteria and some other intracellular pathogens hijack these organelles as a nutrient source and to build up their own lipid inclusions. The mechanisms by which host lipid droplets are captured by the pathogenic bacteria are extremely poorly understood. Using the powerful <italic>D</italic><italic>ictyostelium discoideum</italic>/<italic>M</italic><italic>ycobacterium marinum</italic> infection model, we observed that, immediately after their uptake, lipid droplets translocate to the vicinity of the vacuole containing live but not dead mycobacteria. Induction of lipid droplets in <italic>D</italic><italic>ictyostelium</italic> prior to infection resulted in a vast accumulation of neutral lipids and sterols inside the bacterium‐containing compartment. Subsequently, under these conditions, mycobacteria accumulated much larger lipid inclusions. Strikingly, the <italic>D</italic><italic>ictyostelium</italic> homologue of perilipin and the murine perilipin 2 surrounded bacteria that had escaped to the cytosol of <italic>D</italic><italic>ictyostelium</italic> or microglial BV‐2 cells respectively. Moreover, bacterial growth was inhibited in <italic>D</italic><italic>ictyostelium plnA</italic> knockout cells. In summary, our results provide evidence that mycobacteria actively manipulate the lipid metabolism of the host from very early infection stages.</p> </abstract>