ABSTRACT
Brucella species are facultative intracellular bacteria 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 Brucella are dependent on 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 Brucella and treatment of raft-disrupting agents inhibits bacterial internalisation and intracellular replication. As lipid rafts participate in the signalling pathway in immune cells, entry processes associated with lipid rafts may lead Brucella into compartments that avoid fusion with the lysosomal network in the early stage of infection. Plasma membrane cholesterol of macrophages is also required for bacterial proliferation in mice. Thus, lipid raft microdomains not only influence bacterial internalisation and intracellular replication, but also contribute to the establishment of Brucella infection.
