Subversion of Host Cholesterol by Obligate Intracellular Bacteria
- 1Department of Microbiology and Imunology, Indiana University School of Medicine, USA
Cholesterol is a multifunctional lipid that plays important metabolic and structural roles in the eukaryotic cell. Despite having diverse life styles, the obligate intracellular bacterial pathogens Chlamydia, Coxiella, Anaplasma, Ehrlichia, and Rickettsia all target cholesterol during host cell colonization as a potential source of membrane, as well as a means to manipulate host cell signaling and trafficking. To promote host cell entry, these pathogens utilize cholesterol-rich microdomains known as lipid rafts, which serve as organizational and functional platforms for host signaling pathways involved in phagocytosis. Once a pathogen gains entrance to the intracellular space, it can manipulate host cholesterol trafficking pathways to access nutrient-rich vesicles or acquire membrane components for the bacteria or bacteria-containing vacuole. To acquire cholesterol, these pathogens specifically target host cholesterol metabolism, uptake, efflux, and storage. In this review, we examine the strategies obligate intracellular bacterial pathogens employ to manipulate cholesterol during host cell colonization. Understanding how obligate intracellular pathogens target and use host cholesterol provides critical insight into the host-pathogen relationship.
Keywords: Cholesterol, Chlamydia, Coxiella, Rickettsia, Anaplasma, lipid droplet, lipid raft
Citation: Samanta D, Mulye M, Clemente TM, Justis AV and Gilk S
Received: 06 Jan 2017;
Accepted: 18 Apr 2017.
Edited by:Rey Carabeo, Washington State University, United States of America
Reviewed by:Christopher Thompson, Imperial College London, United Kingdom
Eric Ghigo, Centre national de la recherche scientifique (CNRS), France
Copyright: © 2017 Samanta, Mulye, Clemente, Justis and Gilk. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Stacey Gilk, Indiana University School of Medicine, Department of Microbiology and Imunology, 635 Barnhill Dr., MS 453, Indianapolis, IN, 46202, USA, email@example.com