Chlamydia pneumoniae-Induced Foam Cell Formation Requires MyD88 Dependent and Independent Signaling and is Reciprocally Modulated by LXR Activation
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Summary
It is concluded that C. pneumoniae facilitates foam cell formation via activation of both MyD88-dependent and MyD 88-independent pathways downstream of TLR2 and TLR4 signaling and that TLR3 is not involved in this process.
- Type
- article
- Published
- 2008-11-15
- Cited by
- 94
- References
- 56
- Access
- Open access
- OpenAlex
- https://openalex.org/W1957495725
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:1864387
Keywords
Chlamydia, Cell biology, Receptor, Chemistry, Signal transduction
References
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- TRAM is specifically involved in the Toll-like receptor 4–mediated MyD88-independent signaling pathway
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- Foam Cell Formation Inhibits Growth of Chlamydia pneumoniae but Does Not Attenuate Chlamydia pneumoniae–Induced Secretion of Proinflammatory Cytokines
- TICAM-1, an adaptor molecule that participates in Toll-like receptor 3–mediated interferon-β induction
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- Immunization with the Chlamydia trachomatis major outer membrane protein, using the outer surface protein A of Borrelia burgdorferi as an adjuvant, can induce protection against a chlamydial genital challenge.
- Toll-like receptors.
- Identification of Lps2 as a key transducer of MyD88-independent TIR signalling
- Dual Role of Oxidized LDL on the NF-KappaB Signaling Pathway
- Liver X receptors as integrators of metabolic and inflammatory signaling.
Cited by
- Essential Role of Mitochondrial Antiviral Signaling, IFN Regulatory Factor (IRF)3, and IRF7 in Chlamydophila pneumoniae-Mediated IFN-β Response and Control of Bacterial Replication in Human Endothelial Cells
- Papel de los Liver X Receptors en la activación por IFN-gamma y la proliferación de macrófagos y microglía. Implicaciones en neuroinflamación
- P2X7 Activation of Non-Primed Myeloid Cells Promotes the Shedding of Stimulatory Materials Within Microvesicles
- Mechanisms of bacteria-mediated lipid droplet formation in macrophages
- Effects of gut microbiota on obesity and atherosclerosis via modulation of inflammation and lipid metabolism
- GroEL1, a Heat Shock Protein 60 of Chlamydia pneumoniae, Induces Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Expression in Endothelial Cells and Enhances Atherogenesis in Hypercholesterolemic Rabbits
- Role of gut microbiota in the modulation of atherosclerosis-associated immune response
- The roles of lipid droplets in human infectious disease
- Activation of macrophages by P2X7-induced microvesicles from myeloid cells is mediated by phospholipids and is partially dependent on TLR4
- Infection and Atherosclerosis Development
- MAPK Kinase 3 Potentiates Chlamydia HSP60-Induced Inflammatory Response through Distinct Activation of NF-κB
- Toll-like receptor-dependent lipid body formation in macrophage foam cell formation
- TLR4 rs1927911, but Not TLR2 rs5743708, Is Associated With Atherosclerotic Cerebral Infarction in the Southern Han Population
- Relative roles of various efflux pathways in net cholesterol efflux from macrophage foam cells in atherosclerotic lesions
- Induced expression of lectin-like oxidized ldl receptor-1 in vascular smooth muscle cells following Chlamydia pneumoniae infection and its down-regulation by fluvastatin.
- Role of liver X receptors in cholesterol efflux and inflammatory signaling (Review)
- Interferon regulatory factor 3 protects against adverse neo-intima formation.
- Liver X receptors as regulators of macrophage inflammatory and metabolic pathways.
- The JAK2-Akt-glycogen synthase kinase-3β signaling pathway is involved in toll-like receptor 2-induced monocyte chemoattractant protein-1 regulation
- Chlamydia pneumoniae harness host NLRP3 inflammasome-mediated caspase-1 activation for optimal intracellular growth in murine macrophages.
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