| Literature DB >> 29573124 |
Glenn F W Walpole1,2, Sergio Grinstein1,2,3, Johannes Westman1.
Abstract
Innate immunity relies on the effective recognition and elimination of pathogenic microorganisms. This entails sequestration of pathogens into phagosomes that promptly acquire microbicidal and degradative properties. This complex series of events, which involve cytoskeletal reorganization, membrane remodeling and the activation of multiple enzymes, is orchestrated by lipid signaling. To overcome this immune response, intracellular pathogens acquired mechanisms to subvert phosphoinositide-mediated signaling and use host lipids, notably cholesterol, as nutrients. We present brief overviews of the role of phosphoinositides in phagosome formation and maturation as well as of cholesterol handling by host cells, and selected Salmonella, Shigella, Chlamydia and Mycobacterium tuberculosis to exemplify the mechanisms whereby intracellular pathogens co-opt lipid metabolism in host cells.Entities:
Keywords: bacteria; cholesterol; host-pathogen interactions; lipid droplets; macrophage; membrane trafficking; phagocytosis; phosphoinositides
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Year: 2018 PMID: 29573124 DOI: 10.1002/iub.1737
Source DB: PubMed Journal: IUBMB Life ISSN: 1521-6543 Impact factor: 3.885