Figure 1.

Schematic illustration of lipid fate within the cell. Fatty acids (FAs) bind to their membrane receptors and are translocated to the cytoplasm mediated by the FAs transporters (CD36, FABP, and FATP), where they are chemically modified. First, fatty acyl CoA synthetase adds an acyl CoA moiety to the FA. Then, Carnitine Palmitoyl Transferase 1A (CPT1A) converts the Fatty acyl CoA to Acyl carnitine and facilitates its passage through the mitochondrial outer membrane. Acyl carnitine enters the mitochondrial matrix in exchange for one free carnitine, mediated by Carnitine Acyl Carnitine Transferase (CACT). Carnitine Palmitoyl Transferase 2 (CPTA2) converts acylcarnitine to Acyl-CoA esters that are oxidized to Acyl-CoA that enters the Tricarboxylic Acid Cycle. The increase in the amount of membrane fatty acids receptors leads to the accumulation of cytoplasmic FAs, that are stored as lipid droplets (LDs). Inhibition of the autophagic flux is also responsible for LDs cytoplasmic accumulation. Extracellular pathogens such as P. aeruginosa produce enzymes like Phospholipase A₂ (PLA₂) that convert membrane phospholipids into Prostaglandin E₂ (PGE₂). Also, the spirochete B. burgdorferi can incorporate membrane phospholipids into their own membrane and then, reincorporate them into the cell membrane, leading to the production of antibodies underlying autoimmune responses. Figure generated by BioRender.com.