Essential role for cholesterol in entry of mycobacteria into macrophages.

By John Gatfield, Jean Pieters. Science, 2000

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Mycobacterial persistence requires the utilization of host cholesterol (2008, background): “tuberculosis is initially surrounded by cholesterol-rich plasma membrane after phagocytosis (30), it is unclear whether this membrane composition is maintained in the relatively mature compartment in which replication occurs.”
GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death (2016, neutral): “For extraction of membrane fractions, cells were infected for 15 min with log-phase S. typhimurium , homogenized as described above, and membrane preparation and extraction were performed as described in Gatfield and Pieters (2000).”
The emerging field of lipidomics (2005, background): “Indeed, recognition and uptake of mycobacteria into macrophages involve cholesterol-rich membrane domain”
How can immunology contribute to the control of tuberculosis? (2001, background): “Cholesterol has been shown to act as a docking site for the pathogen, promoting receptor–ligand interaction”
DC-SIGN Is the Major Mycobacterium tuberculosis Receptor on Human Dendritic Cells (2003, background): “Mycobacterial binding to M s occurs in cholesterol-rich domains of the host cell plasma membrane (11) and involves CR3, together with other molecules like MR, CR1, CR4, CD14, surfactant protein (SP)-A receptors, as well as scavenger receptors (12, 13).”