ArticleInflammation2018
Changes in Expression of the Membrane Receptors CD14, MHC-II, SR-A, and TLR4 in Tissue-Specific Monocytes/Macrophages Following Porphyromonas gingivalis-LPS Stimulation.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Periodontitis and Chronic Liver Disease: Mechanistic Insights Focusing onMicroorganisms · 2026Review
- Periodontitis and MASLD: a narrative review of the direct oral-hepatic pathway.Frontiers in cellular and infection microbiology · 2026Review
- Review
- A new direction in periodontitis treatment: biomaterial-mediated macrophage immunotherapy.Journal of nanobiotechnology · 2024Review
- Periodontitis as a promoting factor of T2D: current evidence and mechanisms.International journal of oral science · 2023Review
- Impacts of plasma microbial lipopolysaccharide translocation on B cell perturbations and anti-CD4 autoantibody production in people with HIV on suppressive antiretroviral therapy.Cell & bioscience · 2023Article
- The prohibitin complex regulates macrophage fatty acid composition, plasma membrane packing, and lipid raft-mediated inflammatory signaling.Prostaglandins, leukotrienes, and essential fatty acids · 2023Article
- Sialidase facilitatesFrontiers in cellular and infection microbiology · 2023Article
- TAK-242 Ameliorates Hepatic Fibrosis by Regulating the Liver-Gut Axis.BioMed research international · 2022Article
- Polarized Macrophages in Periodontitis: Characteristics, Function, and Molecular Signaling.Frontiers in immunology · 2021Review
- Oral PathogenMicroorganisms · 2020Article
- Expression of TLR4-PTGE2 signaling genes in atherosclerotic carotid plaques and peripheral blood.Molecular biology reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The aim of the study was to provide a theoretical foundation for understanding the relationship between periodontal diseases and systemic diseases by examining the inflammatory effect of Porphyromonas gingivalis lipopolysaccharide (LPS) on monocytes/macrophages isolated from tissues distinct from the oral cavity in normal and hyperlipidemic New Zealand white rabbits. Macrophages were isolated from four separate tissues (mononuclear cells from blood, alveolar macrophages, peritoneal macrophages, and Kupffer cells) from both normal and hyperlipidemic New Zealand white rabbits. Cells were either stimulated for 24 h in vitro with P. gingivalis-LPS or Escherichia coli-LPS, or were pre-treated with IL-10 before P. gingivalis-LPS treatment. RNA was isolated and the expression of SR-A, TLR4, CD14, and MHC-II measured by RT-PCR. For MHC-II, the suppression effects of P. gingivalis-LPS were similar to the effects of E. coli-LPS in all macrophages examined. In general, the magnitude of the effects of P. gingivalis-LPS on gene expression was lower than that of E. coli-LPS, and there were differences in the relative membrane receptors between the two, implying that the two LPSs stimulate different responses. IL-10 increased the expression of the defensive receptor SR-A and decreased the expression of CD14, TLR4, and the antigen-presenting molecule MHC-II in all types of macrophages examined, regardless of hyperlipidemic state. These data are consistent with an anti-inflammatory effect of IL-10. P. gingivalis-LPS is an activator of gene expression in macrophages isolated from tissues distinct from the oral cavity.
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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.