ArticleCellular microbiology2012
Subversion of NPC1 pathway of cholesterol transport by Anaplasma phagocytophilum.
Article in Cellular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
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- The genus Anaplasma: drawing back the curtain on tick-pathogen interactions.Pathogens and disease · 2021Review
- Functional inhibition or genetic deletion of acid sphingomyelinase bacteriostatically inhibits Anaplasma phagocytophilum infection in vivo.Pathogens and disease · 2021Article
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- Modulation of Host Lipid Pathways by Pathogenic Intracellular Bacteria.Pathogens (Basel, Switzerland) · 2020Review
- Host membrane lipids are trafficked to membranes of intravacuolar bacteriumProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Functional inhibition of acid sphingomyelinase disrupts infection by intracellular bacterial pathogens.Life science alliance · 2019Article
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- Targeting host lipid flows: Exploring new antiviral and antibiotic strategies.Cellular microbiology · 2019Review
- Differential Susceptibility of Male Versus Female Laboratory Mice toTropical medicine and infectious disease · 2018Article
- Alternative Splicing of Differentiated Myeloid Cell Transcripts after Infection byFrontiers in cellular and infection microbiology · 2018Article
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
- Anaplasma phagocytophilum Rab10-dependent parasitism of the trans-Golgi network is critical for completion of the infection cycle.Cellular microbiology · 2016Article
- Economic Game Theory to Model the Attenuation of Virulence of an Obligate Intracellular Bacterium.Frontiers in cellular and infection microbiology · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Intracellular cholesterol amounts, distribution and traffic are tightly regulated to maintain the healthy eukaryotic cell function. However, how intracellular pathogens that require cholesterol, interact with the host cholesterol homeostasis and traffic is not well understood. Anaplasma phagocytophilum is an obligatory intracellular and cholesterol-robbing bacterium, which causes human granulocytic anaplasmosis. Here we found that a subset of cholesterol-binding membrane protein, Niemann-Pick type C1 (NPC1)-bearing vesicles devoid of lysosomal markers were upregulated in HL-60 cells infected with A. phagocytophilum, and trafficked to live bacterial inclusions. The NPC1 localization to A. phagocytophilum inclusions was abolished by low-density lipoprotein (LDL)-derived cholesterol traffic inhibitor U18666A. Studies using NPC1 siRNA and the cell line with cholesterol traffic defect demonstrated that the NPC1 function is required for bacterial cholesterol acquisition and infection. Furthermore, trans-Golgi network-specific soluble N-ethylmaleimide-sensitive factor attachment protein receptors, vesicle-associated membrane protein (VAMP4) and syntaxin 16, which are associated with NPC1 and LDL-derived cholesterol vesicular transport were recruited to A. phagocytophilum inclusions, and VAMP4 was required for bacteria infection. Taken together, A. phagocytophilum is the first example of a pathogen that subverts the NPC1 pathway of intracellular cholesterol transport and homeostasis for bacterial inclusion membrane biogenesis and cholesterol capture.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.