抄録
Intracellular bacteria are capable of surviving inside macrophages and are thought to actively modify their phagosomes to avoid lysosomal fusion for intracellular survival. Both entry and intracellular growth of Legionella and
Brucella are dependent on an interaction with microdomains of the cellular membranes. These microdomains, commonly referred to as lipid rafts, are enriched in glycosylphosphatidylinositol (GPI) -anchored proteins, glycosphingolipids and cholesterol. Lipid raft-associated molecules are selectively incorporated into phagosomes containing
Legionella and Brucella and treatment of raft-disrupting agents inhibits bacterial internalization and intracellular replication. Since lipid rafts involve in signaling pathway in immune cells, entry processes associated with lipid rafts may
lead bacteria into compartments that avoid fusion with the lysosomal network. Plasma membrane cholesterol of
macrophages is also required for bacterial proliferation in mice. Thus, lipid raft microdomains not only influence the
bacterial internalization and intracellular replication, but also contribute to the establishment of bacterial infection.
