Bacterial triacylglycerol lipase

Bacterial triacylglycerol lipases are a diverse class of enzymes (EC 3.1.1.3) secreted by various pathogenic bacteria, including Mycobacterium tuberculosis, Staphylococcus aureus, and Pseudomonas aeruginosa [5, 12, 13]. These enzymes facilitate the hydrolysis of host triacylglycerols into free fatty acids and glycerol, which serve as crucial energy sources and metabolic precursors for the bacteria, particularly during persistent or dormant phases of infection [12, 17]. Beyond nutrient acquisition, bacterial lipases function as essential virulence factors by damaging host cell membranes, promoting tissue invasion, and contributing to the structural integrity of biofilms, which shield pathogens from antibiotics and the host immune response [5, 9, 13]. Therapeutic strategies targeting these lipases aim to attenuate bacterial pathogenicity and survival. Inhibitors like lalistat and tetrahydrolipstatin have demonstrated efficacy in reducing the growth of M. tuberculosis by blocking bacterial hydrolases [2, 11, 12], while farnesol has been explored as an inhibitor of S. aureus lipase to treat skin infections [1, 4]. Furthermore, because these lipases are specifically secreted at infection sites, they are being researched as triggers for smart drug delivery systems that release antimicrobials only in the presence of the pathogen [14]. While primarily viewed as targets for inhibition in infectious diseases, some bacterial lipases are also administered as biotherapeutics in enzyme replacement therapies for conditions like cystic fibrosis or pancreatic insufficiency [21].

Other names

Bacterial lipaseMicrobial lipaseTriacylglycerol acylhydrolaseBacterial glycerol ester hydrolaseBacterial triacylglycerol hydrolase

Inhibition of bacterial lipases prevents the hydrolysis of host-derived lipids, thereby starving the pathogen of fatty acids required for energy and cell wall synthesis; it also disrupts biofilm formation and reduces the production of inflammatory lipid mediators, impairing the bacteria's ability to colonize tissues and evade the host immune system [2, 12].