ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Chlamydia pneumoniae-induced foam cell formation requires MyD88-dependent and -independent signaling and is reciprocally modulated by liver X receptor activation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 86 citations in OpenAlex.
- Lactic Acid Bacteria with Probiotic Potential Regulating Macrophages: Mechanisms, Regulatory Features, and Clinical Applications.Probiotics and antimicrobial proteins · 2026Review
- Feeding the invaders: how metabolic imbalance shapes infection and biofilm development.FEMS microbiology reviews · 2026Review
- The role of TLR4/NF-kB signaling axis in pneumonia: from molecular mechanisms to regulation by phytochemicals.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The role of interferon regulatory factors in atherosclerosis.Frontiers in cardiovascular medicine · 2025Review
- Regulation of ubiquitination in sepsis: from PAMP versus DAMP to peripheral inflammation and cell death.Frontiers in immunology · 2024Review
- Monocyte and Macrophage Lipid Accumulation Results in Down-Regulated Type-I Interferon Responses.Frontiers in cardiovascular medicine · 2022Article
- Lipid droplets and the host-pathogen dynamic: FATal attraction?The Journal of cell biology · 2021Review
- Curcumin affects ox-LDL-induced IL-6, TNF-α, MCP-1 secretion and cholesterol efflux in THP-1 cells by suppressing the TLR4/NF-κB/miR33a signaling pathway.Experimental and therapeutic medicine · 2020Article
- Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020Review
- Chlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.Cell metabolism · 2018Article
- Chlamydia and Lipids Engage a Common Signaling Pathway That Promotes Atherogenesis.Journal of the American College of Cardiology · 2018Article
- Microbial modulation of cardiovascular disease.Nature reviews. Microbiology · 2018Review
- Toll-like receptor 2 downregulates the cholesterol efflux by activating the nuclear factor-κB pathway in macrophages and may be a potential therapeutic target for the prevention of atherosclerosis.Experimental and therapeutic medicine · 2018Article
- Inhibition of TLR4 alleviates the inflammation and apoptosis of retinal ganglion cells in high glucose.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017Article
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
- Macrophage-activating lipopeptide-2 downregulates the expression of ATP-binding cassette transporter A1 by activating the TLR2/NF-кB/ZNF202 pathway in THP-1 macrophages.Acta biochimica et biophysica Sinica · 2016Article
- The Impact of Serum Amyloid P-Component on Gene Expression in RAW264.7 Mouse Macrophages.BioMed research international · 2016Article
- Inflammation-induced foam cell formation in chronic inflammatory disease.Immunology and cell biology · 2015Review
- Infection and Atherosclerosis Development.Archives of medical research · 2015Review
- Role of gut microbiota in the modulation of atherosclerosis-associated immune response.Frontiers in microbiology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Chlamydia pneumoniae is detected by macrophages and other APCs via TLRs and can exacerbate developing atherosclerotic lesions, but how that occurs is not known. Liver X receptors (LXRs) centrally control reverse cholesterol transport, but also negatively modulate TLR-mediated inflammatory pathways. We isolated peritoneal macrophages from wild-type, TLR2, TLR3, TLR4, TLR2/4, MyD88, TRIF, MyD88/TRIF, and IFN regulatory factor 3 (IRF3) KO mice, treated them with live or UV-killed C. pneumoniae in the presence or absence of oxidized LDL, then measured foam cell formation. In some experiments, the synthetic LXR agonist GW3965 was added to macrophages infected with C. pneumoniae in the presence of oxidized LDL. Both live and UV-killed C. pneumoniae induced IRF3 activation and promoted foam cell formation in wild-type macrophages, whereas the genetic absence of TLR2, TLR4, MyD88, TRIF, or IRF3, but not TLR3, significantly reduced foam cell formation. C. pneumoniae-induced foam cell formation was significantly reduced by the LXR agonist GW3965, which in turn inhibited C. pneumoniae-induced IRF3 activation, suggesting a bidirectional cross-talk. We conclude that C. pneumoniae facilitates foam cell formation via activation of both MyD88-dependent and MyD88-independent (i.e., TRIF-dependent and IRF3-dependent) pathways downstream of TLR2 and TLR4 signaling and that TLR3 is not involved in this process. This mechanism could at least partly explain why infection with C. pneumoniae accelerates the development of atherosclerotic plaque and lends support to the proposal that LXR agonists might prove clinically useful in suppressing atherogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.