Expression of perilipin in human promyelocytic cells in response to Anaplasma phagocytophilum infection results in modified lipid metabolism.

J Med Microbiol

Instituto de Investigación en Recursos Cinegéticos IREC (CSIC-UCLM-JCCM), Ronda de Toledo s/n, 13071 Ciudad Real, Spain.

Published: February 2008

AI Article Synopsis

  • - Anaplasma phagocytophilum is a tick-borne pathogen that causes various diseases in humans and animals, and it relies on host lipids for its infection process.
  • - A previous study identified the perilipin (PLIN) gene as being differentially expressed in response to A. phagocytophilum infection, suggesting it plays a role in lipid metabolism.
  • - This study found that A. phagocytophilum increases PLIN mRNA levels, which aids in its infection of human HL-60 cells, providing insight into how the pathogen manipulates lipid metabolism for its benefit.

Article Abstract

The obligate intracellular pathogen Anaplasma phagocytophilum is transmitted by ticks and causes human granulocytic anaplasmosis, tick-borne fever of ruminants, and equine and canine granulocytic anaplasmosis. In a previous study, the perilipin (PLIN) gene was identified as one of the genes differentially expressed in human promyelocytic HL-60 cells in response to infection with A. phagocytophilum. PLIN is a major adipocyte lipid droplet-associated phosphoprotein that plays a central role in lipolysis and cholesterol synthesis. Host cholesterol and other lipids are required by A. phagocytophilum for infection and multiplication in human cells. In this study, it was hypothesized that PLIN may be involved in infection of human HL-60 cells by A. phagocytophilum. To test this hypothesis, a combination of real-time RT-PCR, immunofluorescence and RNA interference was used to study the expression of PLIN. The results of these studies demonstrated that A. phagocytophilum modulates lipid metabolism by increasing PLIN mRNA levels and facilitates infection of HL-60 cells. The results of these studies expand our knowledge of the role of lipid metabolism in A. phagocytophilum infection and multiplication in HL-60 cells and suggest a mechanism by which A. phagocytophilum modulates lipid metabolism.

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http://dx.doi.org/10.1099/jmm.0.47504-0DOI Listing

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