International Journal of Infection 2025; 9(3) September-December: 83-86
PHOSPHATIDYLCHOLINE INFLUENCES MEMBRANE PERMEABILITY AND PATHOGEN PENETRATION
Tocco P. Phosphatidylcholine influences membrane permeability and pathogen penetration. International Journal of Infection. 2025;9(3):83-86.
P. Tocco*
Unità Operativa Complessa, Neurology and Stroke Unit, Asl Pescara, Pescara, Italy.
*Correspondence to:
Dr. Pierluigi Tocco,
UOC Neurology and Stroke Unit,
Asl Pescara P.O.,
Pescara, Italy.
e-mail: pxtocco@gmail.com
ABSTRACT
Phosphatidylcholine (PC) is an important membrane phospholipid involved in microorganism-host interactions. Choline is a precursor to acetylcholine, which is is a precursor molecule to PC. PC is an essential nutrient that has structural, functional, and cell membrane integrity roles. It plays a role in the interaction between microorganisms and host cells, influencing the course of infection. It acts as a barrier and influences cell membrane permeability and the penetration of microorganisms. Lipid mediators such as lysophosphatidylcholine (LPC) participate in the inflammatory process by causing complement activation and the recruitment of neutrophils and macrophages to the site of infection with the production of pro-inflammatory cytokines, although some species of LPC or PC may also have anti-inflammatory activity. LPC inhibitors reduce the pathogenic effect of microorganisms, and PC act as an anti-inflammatory.
KEYWORDS: Phosphatidylcholine, phospholipid, lipid mediator, infection, pathogen
INTRODUCTION
Phosphatidylcholine (PC) belongs to an important class of membrane phospholipids involved in pathogen-host interactions (1). PC is a phospholipid that contains choline as a functional group. Structurally, PC consists of a polar head (choline linked to a phosphate group) and two hydrophobic fatty acid tails (2). Choline is a precursor molecule of PC, which is an essential nutrient involved in numerous brain functions (3). One of its main roles is serving as a precursor to acetylcholine, an essential neurotransmitter for cognitive function (4).
Genes involved in PC biosynthesis (such as pcs, pmtA, choA/B) are used to study lipid transcriptional regulation (5). PC plays structural and functional roles, influencing the fluidity, curvature, and integrity of the cell membrane (6). Interactions between microorganisms and host cells are mediated by PC metabolism, which is influenced by viruses, bacteria, and parasites to promote infection (7) (Table I). PC is a major phospholipid in cell membranes and plasma lipoproteins and is composed of glycerol, fatty acids, choline, and a phosphate group, and its degradation products are implicated in inflammatory reactions (8,9). PC can be synthesized de novo through the CDP-choline pathway (or Kennedy pathway), which is the main synthesis pathway, or through PC methylation (10).
Table I. Phosphatidylcholine (PC) in microorganisms.
| Characteristics: | – Bacteria, Archaea, Unicellular eukaryotes (yeasts, protozoa) |
| – Very abundant | |
| – Presence of PC: In ~12% of species (mainly pathogens and symbionts) | |
| – Type of lipid bond: fatty acid esters with glycerol | |
| – Esters of fatty acids with glycerol | |
| – Biosynthetic pathways: CDP–choline (Kennedy pathway) | |
| Main functions: | – Adhesion, virulence, host mimicry, membrane stability |
| – Thermal stability, environmental adaptation | |
| – Membrane integrity, secretion, division, metabolism Lipid | |
| Molecular role: | – Bacterial-host interaction, regulation of secretion systems, extreme adaptation (high temperature, pH, salinity), regulation of vesicle trafficking and endoplasmic reticulum stress |
DISCUSSION
PC plays a key role in the host barrier and signalling in infections, influencing both cell membrane permeability and microorganism penetration (11). Lipid mediators such as lysophosphatidylcholine (LPC) mediate the inflammatory response by attracting immune cells such as neutrophils and macrophages to the site of infection (12). Complement, which participates in the immune response, is also activated in the inflammatory response (13).
Many pathogens exploit PC by degrading it to promote infection. Bacteria such as Pseudomonas aeruginosa and Streptococcus pneumoniae produce phospholipases C or D that degrade PC, damaging host membranes and obtaining choline (14). Other bacteria such as Legionella pneumophila and Helicobacter pylori modify PC to evade immune recognition (15). Some viruses, such as influenza virus, hepatitis C virus, and SARS-CoV-2, also act on PC-rich membranes to create replication vacuoles (16). Differential membrane PC formation can influence the assembly and release of viral particles (17). In pathogen-host interactions, PC improves the ability of pathogenic bacteria to infect eukaryotic cells, and mutations in PC synthesis pathways are exploited to modulate immune responses or lipid production (18) (Table II). In yeast, PC synthesis pathways are exemplary models for the study of lipid metabolism and gene regulation (19,20).
Table II. Biological roles of phosphatidylcholine (PC).
| In bacteria: | – Essential for secretion, division and lipid metabolism |
| – Promotes interaction with eukaryotic cells | |
| – Present in pathogens or symbionts (e.g., Brucella, Rhizobium) | |
| – Helps camouflage the host membrane | |
| – Regulates protein stability and secretion | |
| In eukaryotes: | – Major membrane phospholipid |
| – Maintains fluidity and asymmetry of the bilayer |
Parasites such as Leishmania and Trypanosoma alter PC metabolism to survive macrophage phagocytosis (21). LPC is produced by PC through phospholipase A₂, a molecule implicated in the inflammatory process mediated by cytokines, including IL-1 and TNF. These cytokines activate endothelial cells and leukocytes to produce inflammatory molecules (22). However, some species of LPC or PC may also have anti-inflammatory activity and limit tissue damage (23). This depends on the degree and type of infection. Therapy with phospholipase inhibitors can reduce bacterial virulence, while PC supplementation can help stabilize membranes and reduce inflammation (24).
CONCLUSIONS
The metabolic targets of some PC synthesis pathways are essential for viral or bacterial replication and therefore can be used as potential drug targets. PC improves the ability of pathogenic bacteria to infect eukaryotic cells, and its alteration leads to endoplasmic reticulum stress and mitochondrial dysfunction. PC dysregulation is treated with phospholipase inhibitors, PC supplementation, and specific metabolic targets for PC synthesis. Exploring the evolution of metabolic pathways in microorganisms is important, and analyzing PC-deficient mutants helps to understand the role of phospholipids in membrane function.
Conflict of interest
The author declares that they have no conflict of interest.
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