Fifteen years ago, in a series of elegant studies, Hackstadt and colleagues showed that the obligate intracellular bacteria Chlamydia trachomatis save on their lipid needs by incorporating sphingomyelins (SMs) made by their host. Shortly after, Hatch and McClarty’s teams reported that several eukaryotic glycerophospholipids are also trafficked from the host to the bacteria, which replace host-synthesized straight-chain fatty acids by their own branched-chain fatty acids. Even cholesterol, a lipid rarely found in bacteria, was shown to accumulate in Chlamydia. As a result of this intense exploitation of host lipids, the composition of the bacterial membrane is closer to that of a eukaryotic cell than to that of a prokaryote.
Throughout their developmental cycle, chlamydiae reside within a membrane-bounded compartment, the inclusion. How they acquire host lipids remains an open question. Possible mechanisms studied so far involve vesicular trafficking from host compartments, including vesicular traffic out of the Golgi apparatus, fusion with multivesicular body–derived vesicles, and engulfment of lipid droplets.