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Cardiolipin remodeling in eukaryotic cells infected with Chlamydia trachomatis is linked to elevated mitochondrial
1Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada. hatchgm@ms.umanitoba.ca
Abstract:
Cardiolipin remodeling in mammalian eukaryotic cells was examined subsequent to infection with Chlamydia trachomatis, an intracellular parasite of eukaryotic cells. HeLa cells were labeled for 6 h with [1-14C]myristate or [1-14C]palmitate or [1-14C]oleate 20 h post infection with C. trachomatis and the radioactivity incorporated into glycerophospholipids examined. Chlamydia infection resulted in a 2-4 fold elevation of radioactive myristate, palmitate or oleate incorporation into phosphatidylethanolamine, phosphatidylcholine, phosphatidylserine and phosphatidylinositiol compared to mock-infected cells. However, a 4-10 fold elevation in radioactivity incorporated into the mitochondrial glycerophospholipids phosphatidylglycerol and cardiolipin was observed in chlamydia-infected cells compared to mock-infected controls. Glycerophospholipid remodeling in CCL16-B2 cells, a mitochondrial respiration mutant with elevated glycerophospholipid metabolism, was compared to its parental cell line CCL16-B1 infected with C. trachomatis. Infection of the wild type CCL16-B1 cells with C. trachomatis resulted in an almost identical pattern of [1-14C]-palmitate labeling of glycerophospholipids compared to the uninfected mitochondrial mutant CCL16-B2 cells. The results suggest that cardiolipin, and glycerophospholipid, fatty acid molecular remodeling in eukaryotic cells infected with C. trachomatis may be linked to an elevation in mitochondrial metabolism.