Hanski, Leena

Miettinen, Ilkka

Nyman, Tuula

Savijoki, Kirsi

Taavitsainen, Eveliina

English

Helsingin yliopiston digitaalinen arkisto

Abstract to be presented at World Microbe Forum 2021  A ProteomicS study on Chlamydia pneumoniae -Induced Changes in Macrophages  Eveliina Taavitsainen1, Ilkka Miettinen1, Kirsi Savijoki1,2, Tuula Nyman3 and Leena Hanski1  1Faculty of Pharmacy, 2Faculty of Agriculture and Forestry, University of Helsinki, Finland, 3Department of Immunology, University of Oslo and Oslo University Hospital, Norway  BACKGROUND: Chlamydia (Chlamydophila) pneumoniae is a small, morphologically and metabolically distinct gram-negative bacterium with obligately intracellular life cycle. It is the causative agent of human respiratory infections ranging from pneumoniae to dry cough, with 60-80% global seroprevalence. The tendency of C. pneumoniae to persist in macrophages even in the absence of exogenous triggers is well known, but the underlying host-chlamydial interactions driving the bacterial stress response remain elusive. OBJECTIVES: In this work, we describe changes in macrophage intracellular signaling pathways induced by C. pneumoniae infection. METHODS: Human THP-1-derived macrophages were infected with C. pneumoniae cardiovascular isolate CV6 and total cellular protein lysates were collected at 48 h and 72 h post-infection. Label-free quantitative proteome analysis combined with pathway analysis tools were used to identify patterns of differentially expressed proteins between infected and noninfected macrophages. RESULTS: A total of 2136 macrophage proteins were quantified in at least two out of three replicates for each sample. A one-way ANOVA (permutation-based false discovery rate 0.10) identified 214 proteins with significantly and consistently altered expression between the conditions. At 48 h post-infection, pathways associated with the positive regulation of NF-kappaB were stressed, while the negative regulation of cell cycle control was prominent at both 48 h and 72 h. The upregulation of S100A8 and S100A9 calcium-binding proteins, osteopontin and purine nucleoside phosphorylase LACC1 underlined the proinflammatory consequences of the infection, while the elevated NF-kappaB p100 levels in the infected macrophages implied interactions also with the noncanonical NF-kappaB pathway. Infection-induced changes in macrophage lipid metabolism were indicated by the upregulation of the scavenger receptor CD36 (cluster of differentiation 36) and ACAD10 (acyl coenzyme A dehydrogenase family member 10). The downregulated proteins were dominated by the mini chromosome maintenance (MCM) complex proteins 2 – 6, gamma glutamyl transferase 1 (GGT1) and fatty acid-binding protein 4 (FABP4). Collectively, this work represents a first proteomics study on C. pneumoniae – macrophage interactions and identifies several host cell proteins with yet unreported expression changes upon C. pneumoniae infection.   Acknowledgement: This work has been funded by Academy of Finland grant 333291 to LH and Finnish Cultural Foundation personal grant to ET. 

A ProteomicS study on Chlamydia pneumoniae -Induced Changes in Macrophages

https://helda.helsinki.fi/bitstream/10138/332229/1/Taavitsainen_et_al_WMF2021_abstract.pdf

A ProteomicS study on Chlamydia pneumoniae -Induced Changes in Macrophages

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