Chlamydia pneumoniae Interferes with Macrophage Differentiation and Cell Cycle Regulation to Promote Its Replication

Show full item record



Permalink

http://hdl.handle.net/10138/343679

Citation

Taavitsainen-Wahlroos , E , Miettinen , I , Kortesoja , M , Reigada , I , Savijoki , K , Nyman , T A & Hanski , L 2022 , ' Chlamydia pneumoniae Interferes with Macrophage Differentiation and Cell Cycle Regulation to Promote Its Replication ' , Cellular Microbiology , vol. 2022 , 9854449 . https://doi.org/10.1155/2022/9854449

Title: Chlamydia pneumoniae Interferes with Macrophage Differentiation and Cell Cycle Regulation to Promote Its Replication
Author: Taavitsainen-Wahlroos, Eveliina; Miettinen, Ilkka; Kortesoja, Maarit; Reigada, Inés; Savijoki, Kirsi; Nyman, Tuula Anneli; Hanski, Leena
Contributor organization: Faculty of Pharmacy
Division of Pharmaceutical Biosciences
Helsinki Institute of Sustainability Science (HELSUS)
Explorations of Anti Infectives
Pharmaceutical Design and Discovery group
Department of Food and Nutrition
The Academic Outreach Network
Helsinki One Health (HOH)
Divisions of Faculty of Pharmacy
Drug Research Program
Date: 2022-04-11
Language: eng
Number of pages: 19
Belongs to series: Cellular Microbiology
ISSN: 1462-5814
DOI: https://doi.org/10.1155/2022/9854449
URI: http://hdl.handle.net/10138/343679
Abstract: Chlamydia pneumoniae is a ubiquitous intracellular bacterium which infects humans via the respiratory route. The tendency of C. pneumoniae to persist in monocytes and macrophages is well known, but the underlying host-chlamydial interactions remain elusive. In this work, we have described changes in macrophage intracellular signaling pathways induced by C. pneumoniae infection. Label-free quantitative proteome analysis and pathway analysis tools were used to identify changes in human THP-1-derived macrophages upon C. pneumoniae CV6 infection. At 48-h postinfection, pathways associated to nuclear factor kappa B (NF-kappa B) regulation were stressed, while negative regulation on cell cycle control was prominent at both 48 h and 72 h. Upregulation of S100A8 and S100A9 calcium binding proteins, osteopontin, and purine nucleoside hydrolase, laccase domain containing protein 1 (LACC1) underlined the proinflammatory consequences of the infection, while elevated NF-kappa B2 levels in infected macrophages indicates interaction with the noncanonical NF-kappa B pathway. Infection-induced alteration of cell cycle control was obvious by the downregulation of mini chromosome maintenance (MCM) proteins MCM2-7, and the significance of host cell cycle regulation for C. pneumoniae replication was demonstrated by the ability of a cyclin-dependent kinase (CDK) 4/6 inhibitor Palbociclib to promote C. pneumoniae replication and infectious progeny production. The infection was found to suppress retinoblastoma expression in the macrophages in both protein and mRNA levels, and this change was reverted by treatment with a histone deacetylase inhibitor. The epigenetic suppression of retinoblastoma, along with upregulation of S100A8 and S100A9, indicate host cell changes associated with myeloid-derived suppressor cell (MDSC) phenotype.
Subject: 317 Pharmacy
FACTOR-KAPPA-B
IN-VITRO
UP-REGULATION
SIGNAL-TRANSDUCTION
ENDOTHELIAL-CELLS
INFECTION
GAMMA
PROTEIN
EXPRESSION
RESPONSES
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


Files in this item

Total number of downloads: Loading...

Files Size Format View
9854449.pdf 1.247Mb PDF View/Open

This item appears in the following Collection(s)

Show full item record