ArticleInflammation2012
Oxidized LDLs inhibit TLR-induced IL-10 production by monocytes: a new aspect of pathogen-accelerated atherosclerosis.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Identification of a leucine-mediated threshold effect governing macrophage mTOR signalling and cardiovascular risk.Nature metabolism · 2024Article
- Monocyte Phenotypes and Physical Activity in Patients with Carotid Atherosclerosis.Antioxidants (Basel, Switzerland) · 2022Article
- Relationship between Brain Metabolic Disorders and Cognitive Impairment: LDL Receptor Defect.International journal of molecular sciences · 2022Review
- Corilagin Ameliorates Atherosclerosis in Peripheral Artery Disease via the Toll-Like Receptor-4 Signaling PathwayFrontiers in immunology · 2020Article
- Phenotype and Response to PAMPs of Human Monocyte-Derived Foam Cells Obtained by Long-Term Culture in the Presence of oxLDLs.Frontiers in immunology · 2020Article
- Monocyte Subsets in Atherosclerosis and Modification with Exercise in Humans.Antioxidants (Basel, Switzerland) · 2018Review
- Role of TLR4 and miR-155 in peripheral blood mononuclear cell-mediated inflammatory reaction in coronary slow flow and coronary arteriosclerosis patients.Journal of clinical laboratory analysis · 2018Article
- Pro-resolving mediators in the regulation of periodontal disease.Molecular aspects of medicine · 2017Review
- Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling.Cellular and molecular life sciences : CMLS · 2015Review
- Porphyromonas gingivalis exacerbates ligature-induced, RANKL-dependent alveolar bone resorption via differential regulation of Toll-like receptor 2 (TLR2) and TLR4.Infection and immunity · 2014Article
- Serum osteocalcin level and its association with carotid atherosclerosis in patients with type 2 diabetes.Cardiovascular diabetology · 2013Article
- Article
- Hepatitis B virus induces expression of cholesterol metabolism-related genes via TLR2 in HepG2 cells.World journal of gastroenterology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely accepted that oxidized low-density lipoproteins and local infections or endotoxins in circulation contribute to chronic inflammatory process at all stages of atherosclerosis. The hallmark cells of atherosclerotic lesions-monocytes and macrophages-are able to detect and integrate complex signals derived from lipoproteins and pathogens, and respond with a spectrum of immunoregulatory cytokines. In this study, we show strong inhibitory effect of oxLDLs on anti-inflammatory interleukin-10 production by monocytes responding to TLR2 and TLR4 ligands. In contrast, pro-inflammatory tumor necrosis factor secretion was even slightly increased, when stimulated with lipopolysaccharide from Porphyromonas gingivalis-an oral pathogen associated with atherosclerosis. The oxLDLs modulatory activity may be explained by altered recognition of pathogen-associated molecular patterns, which involves serum proteins, particularly vitronectin. We also suggest an interaction between vitronectin receptor, CD11b, and TLR2. The presented data support a novel pathway for pathogen-accelerated atherosclerosis, which relies on oxidized low-density lipoprotein-mediated modulation of anti-inflammatory response to TLR ligands.
Indexed as
Identifiers
What OpenQuestion holds
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.