A1 Refereed original research article in a scientific journal
ABC-cassette transporter 1 (ABCA1) expression in epithelial cells in Chlamydia pneumoniae infection
Authors: Korhonen JT, Olkkonen VM, Lahesmaa R, Puolakkainen M
Publisher: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Publishing place: LONDON; 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
Publication year: 2013
Journal: Microbial Pathogenesis
Journal name in source: Microbial pathogenesis
Journal acronym: Microb.Pathog.
Volume: 61-62
First page : 57
Last page: 61
Number of pages: 5
ISSN: 0882-4010
DOI: https://doi.org/10.1016/j.micpath.2013.05.006(external)
Abstract
ATP-binding cassette transporter A1 (ABCA1) mediates reverse cholesterol transport and innate immunity response in different cell types. We have investigated the regulation of ABCA1 expression in response to intracellular Chlamydia pneumoniae infection in A549 epithelial lung carcinoma cells. C. pneumoniae infection decreased ABCA1 expression in A549 cells, and the activity of the ABCA1 promoter was decreased. The decreased promoter activity was dependent on its E-box and GnT-box elements of the promoter. Chlamydial growth was decreased in ABCA1-silenced epithelial lung carcinoma cells. These data indicate an important role for ABCA1 in intracellular bacterial infection. (c) 2013 Elsevier Ltd. All rights reserved.
ATP-binding cassette transporter A1 (ABCA1) mediates reverse cholesterol transport and innate immunity response in different cell types. We have investigated the regulation of ABCA1 expression in response to intracellular Chlamydia pneumoniae infection in A549 epithelial lung carcinoma cells. C. pneumoniae infection decreased ABCA1 expression in A549 cells, and the activity of the ABCA1 promoter was decreased. The decreased promoter activity was dependent on its E-box and GnT-box elements of the promoter. Chlamydial growth was decreased in ABCA1-silenced epithelial lung carcinoma cells. These data indicate an important role for ABCA1 in intracellular bacterial infection. (c) 2013 Elsevier Ltd. All rights reserved.