Role of lipid rafts in persistent Helicobacter pylori infection: a narrative review

Abstract

Background and Objective: The distribution of components in the cell membrane is not uniform, but is organized into specific functional microdomains, known as "lipid rafts". These lipid rafts consist of cholesterol, sphingolipids, and various proteins. Studies have shown that lipid rafts contain multiple proteins that are closely related to signal transduction and immune response. Furthermore, lipid rafts are the sites where a variety of pathogens invade the cells, and are associated with the persistent infection of some pathogens, especially Helicobacter pylori (Hp). We are going to explore a new method to treat Hp by discussing the important role of lipid rafts in Hp persistent infection.Methods: Papers on lipid rafts were retrieved to analyze the evolution of the definition of lipid raft, research techniques, and studies on the correlation of lipid rafts with pathogens infecting host cells.

Inhibitory and Injury-Protection Effects of O-Glycan on Gastric Epithelial Cells Infected with Helicobacter pylori

“…As a nanoscale domain on the cell membrane, lipid rafts are rich in cholesterol and sphingomyelin, contain a variety of receptors, channel proteins, and signaling molecules, and serve as a functional platform for the interactions of protein-protein, protein-lipid, and lipid-lipid ( 27 ). Lipid rafts are involved in the regulation of several processes such as pathogen adhesion, cellular signaling, and immune response, and are the key cellular domain mediating H. pylori infection of gastric epithelial cells and causing inflammatory responses ( 12 ). H. pylori infection stimulates the recruitment and activation of immune cells such as Th1, in which Th1-dominant CD4 + T cells facilitate the inflammatory responses in gastric tissue by secreting IFN-γ ( 28 ), thereby playing a decisive role in controlling bacterial load and infection of H. pylori ( 29 , 30 ).…”

“…In the early stage of infection, H. pylori was reported to secret cholesterol-α-glucosyltransferase (CGT) interacts with specialized cholesterol-rich membrane microdomains, known as lipid rafts ( 10 ), thereby promoting the recruitment of binding antigens in lipid rafts and further enhancing the colonization of H. pylori ( Fig. 1A and B ) ( 11 , 12 ).…”

Trained Immunity and Trained Tolerance: The Case of Helicobacter pylori Infection

“…Therefore, the latter, unlike the former, has a protective (immune evasion) action for the bacterium. The association of H. pylori with lipid rafts is particularly intriguing: These are dynamic cholesterol-rich membrane subdomains, containing specific proteins that play crucial roles in signal transduction, membrane trafficking, and protein sorting [ 60 ]. Among the latter, there are pattern recognition receptors (PRRs), such as toll-like receptors (TLRs) and C-type lectin receptors (CLRs), which are critical for detecting pathogen-associated molecular patterns (PAMPs).…”

“…Upon activation, these cells undergo dynamic changes in membrane lipid composition and organization, leading to the redistribution of lipid rafts and the clustering of immune receptors at the site of pathogen entry. The ability of H. pylori to disrupt lipid rafts in macrophages and NK cells may be an important mechanism to escape immune detection and promote survival and replication [ 60 , 61 ]. Given that the spatial organization of lipid rafts in macrophages is known to be under epigenetic control [ 62 ], it would be interesting to investigate whether H. pylori is able to train immune cells to tolerate the pathogen following sustained interactions with the host.…”

Biosynthesis, structure and biological function of cholesterol glucoside in Helicobacter pylori: A review

“…[39,40] Lipid rafts have been found on the cell membranes of prokaryotes such as E coli , [41] Staphylococcus aureus , [42] and Borrelia burgdorferi . [43] Lipid rafts are the entrance of many pathogens including H pylori [44,45] and the “bridge” for these pathogens to invade host cells, and can affect the integrity and morphology of membranes. [46] Huang et al [29] separated all lipids in H pylori , including αCG, αCAG, αCPG and cholesterol, and found that αCAG, αCPG and cholesterol all could form an ordered and disordered lipid bilayer structure on the membrane, very similar to the lipid rafts in eukaryotic cells, but there were some differences in the stability of the rafts: αCAG being the strongest and αCPG the weakest.…”