ArticleCellular microbiology2013
Transcription factor complex AP-1 mediates inflammation initiated by Chlamydia pneumoniae infection.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
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- Resolvin D1 alleviates lipopolysaccharide-inducedBioImpacts : BI · 2025Article
- A distinct metabolic and epigenetic state drives trained immunity in HSC-derived macrophages from autoimmune mice.Cell stem cell · 2024Article
- Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3.Nature communications · 2024Article
- Statin prevents cancer development in chronic inflammation by blocking interleukin 33 expression.Nature communications · 2024Article
- Immunomodulatory Effects of Fluoroquinolones in Community-Acquired Pneumonia-Associated Acute Respiratory Distress Syndrome.Biomedicines · 2024Review
- CRIF1 deficiency induces FOXP3Science advances · 2024Article
- Temporal dynamics of the bat wing transcriptome: Insight into gene-expression changes that enable protection against pathogen.Virulence · 2023Article
- Role of ST6GAL1 and ST6GAL2 in subversion of cellular signaling during enteroaggregative Escherichia coli infection of human intestinal epithelial cell lines.Applied microbiology and biotechnology · 2023Article
- Mechanisms underlying the Effects of Heat Stress on Intestinal Integrity, Inflammation, and Microbiota in Chickens.The journal of poultry science · 2023Review
- Single-cell transcriptomic, transcriptomic, and metabolomic characterization of human atherosclerosis.Annals of translational medicine · 2022Article
- P. aeruginosa type III and type VI secretion systems modulate early response gene expression in type II pneumocytes in vitro.BMC genomics · 2022Article
- Investigating the in vitro steatotic mixture effects of similarly and dissimilarly acting test compounds using an adverse outcome pathway-based approach.Archives of toxicology · 2022Article
- Article
- HIF-1α/JMJD1A signaling regulates inflammation and oxidative stress following hyperglycemia and hypoxia-induced vascular cell injury.Cellular & molecular biology letters · 2021Article
- Efficient In Vitro and In Vivo Anti-Inflammatory Activity of a Diamine-PEGylated Oleanolic Acid Derivative.International journal of molecular sciences · 2021Article
- Dual RNA-seq analysis of in vitro infection multiplicity and RNA depletion methods in Chlamydia-infected epithelial cells.Scientific reports · 2021Article
- Phytobiotics to improve health and production of broiler chickens: functions beyond the antioxidant activity.Animal bioscience · 2021Article
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Chlamydia pneumoniae is responsible for a high prevalence of respiratory infections worldwide and has been implicated in atherosclerosis. Inflammation is regulated by transcription factor (TF) networks. Yet, the core TF network triggered by chlamydiae remains largely unknown. Primary human coronary artery endothelial cells were mock-infected or infected with C. pneumoniae to generate human transcriptome data throughout the chlamydial developmental cycle. Using systems network analysis, the predominant TF network involved receptor, binding and adhesion and immune response complexes. Cells transfected with interfering RNA against activator protein-1 (AP-1) members FOS, FOSB, JUN and JUNB had significantly decreased expression and protein levels of inflammatory mediators interleukin (IL)6, IL8, CD38 and tumour necrosis factor compared with controls. These mediators have been shown to be associated with C. pneumoniae disease. Expression of AP-1 components was regulated by MAPK3K8, a MAPK pathway component. Additionally, knock-down of JUN and FOS showed significantly decreased expression of Toll-like receptor (TLR)3 during infection, implicating JUN and FOS in TLR3 regulation. TLR3 stimulation led to elevated IL8. These findings suggest that C. pneumoniae initiates signalling via TLR3 and MAPK that activate AP-1, a known immune activator in other bacteria not previously shown for chlamydiae, triggering inflammation linked to C. pneumoniae disease.
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