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Host cell phospholipids are trafficked to and then modified by Chlamydia trachomatis
J L Wylie1, G M Hatch, G McClarty
1Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada.
Journal of Bacteriology
|December 11, 1997
Summary
Chlamydia trachomatis traffics eukaryotic lipids from host cells, modifying them by replacing fatty acids. This reveals new insights into host-pathogen lipid metabolism and host-pathogen interactions.
Area of Science:
- Microbiology
- Cell Biology
- Biochemistry
Background:
- Limited knowledge exists on eukaryotic lipid trafficking to intracellular pathogens.
- Chlamydia trachomatis, an obligate intracellular parasite, contains host-derived lipids but transfer mechanisms were unclear.
Purpose of the Study:
- To demonstrate and characterize the trafficking of eukaryotic glycerophospholipids from host cells to Chlamydia trachomatis.
- To investigate the modification and synthesis of phospholipids by C. trachomatis.
Main Methods:
- Tracking radiolabeled precursors to assess glycerophospholipid incorporation.
- Monitoring the transfer and conversion of host phosphatidylserine to phosphatidylethanolamine in chlamydiae.
- Assessing trafficking in the presence of brefeldin A and in mutant cell lines.
Main Results:
- Eukaryotic glycerophospholipids are successfully trafficked from host cells to C. trachomatis.
- Trafficking is independent of Golgi function and nonspecific phospholipid transfer proteins.
- C. trachomatis modifies host phospholipids by altering fatty acid composition.
- C. trachomatis retains the ability for de novo synthesis of prokaryotic phospholipids.
Conclusions:
- This study provides novel insights into chlamydial phospholipid metabolism and eukaryotic lipid trafficking.
- The findings enhance understanding of the metabolic associations between intracellular bacteria and host cells.
- The results shed light on the evolutionary adaptations enabling intimate host-pathogen interactions.