ArticleOral microbiology and immunology2009
Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression.
Article in Oral microbiology and immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- The Role of the Oral Microbiome in the Development and Treatment of Periodontal Disease: Functional Meta-Omics Evidence.Current microbiology · 2026Review
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- Tissue engineered bovine saphenous vein extracellular matrix scaffolds produced via antigen removal achieve high in vivo patency rates.Acta biomaterialia · 2021Article
- Article
- Macrophage scavenger receptor 1 contributes to pathogenesis of fulminant hepatitis via neutrophil-mediated complement activation.Journal of hepatology · 2018Article
- Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy.Scientific reports · 2017Article
- Signaling events in pathogen-induced macrophage foam cell formation.Pathogens and disease · 2016Article
- Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.Journal of periodontal research · 2015Article
- Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms.Current oral health reports · 2014Article
- Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3.Innate immunity · 2014Article
- RANKL expression in periodontal disease: where does RANKL come from?BioMed research international · 2014Review
- Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation.Molecular oral microbiology · 2013Article
- Immune response of macrophages from young and aged mice to the oral pathogenic bacterium Porphyromonas gingivalis.Immunity & ageing : I & A · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
introductionPorphyromonas gingivalis is a periodontopathic bacterium closely associated with generalized aggressive periodontal disease. Pattern recognition receptors (PRRs) participate in host response to this organism. It is likely that PRRs not previously recognized as part of the host response to P. gingivalis also participate in host response to this organism. METHODS AND
resultsEmploying qRT-PCR, we observed increased msr1 gene expression at 2, 6, and 24 h of culture with P. gingivalis strain 381. Flow cytometry revealed increased surface expression of SR-A protein by the 24 h time point. Macrophages cultured with an attachment impaired P. gingivalis fimA- mutant (DPG3) expressed intermediate levels of SR-A expression. Heat-killed P. gingivalis stimulated SR-A expression similar to live bacteria, and purified P. gingivalis capsular polysaccharide stimulated macrophage SR-A expression, indicating that live whole organisms are not necessary for SR-A protein expression in macrophage response. As SR-A is known to play a role in lipid uptake by macrophages, we tested the ability of low-density lipoprotein (LDL) to influence the SR-A response of macrophages to P. gingivalis, and observed no effect of LDL on P. gingivalis-elicited SR-A expression. Lastly, we observed that SR-A knockout (SR-A(-/-)) mouse macrophages produced significantly more tumor necrosis factor (TNF)-alpha than wild type mouse macrophages cultured with P. gingivalis.
conclusionThese data identify that SR-A is expressed by macrophages in response to P. gingivalis, and support that this molecule plays a role in TNF-alpha production by macrophages to this organism.
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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.