ArticleCell death & disease2017
Porphyromonas gingivalis gingipains cause defective macrophage migration towards apoptotic cells and inhibit phagocytosis of primary apoptotic neutrophils.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 47 citations in OpenAlex.
- P. gingivalis-host interactions direct antibiotic adjuvants for periodontitis antimicrobial therapy.International journal of oral science · 2026Article
- The mediating effect of triglycerides and related indices on the association between polycyclic aromatic hydrocarbons and oral health in adults aged ≥ 45 years from the national health and nutrition examination survey 2003-2016.Lipids in health and disease · 2026Article
- Review
- Gingipains protect Porphyromonas gingivalis from macrophage-mediated phagocytic clearance.PLoS pathogens · 2025Article
- Periodontal pathogens and cancer development.Periodontology 2000 · 2024Review
- Colorimetric sensing for translational applications: from colorants to mechanisms.Chemical Society reviews · 2024Review
- Sialidase facilitatesFrontiers in cellular and infection microbiology · 2023Article
- Review
- Porphyromonas gingivalis Activation of Tumor-Associated Macrophages via DOK3 Promotes Recurrence of Oral Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- COR388 (atuzaginstat): an investigational gingipain inhibitor for the treatment of Alzheimer disease.Expert opinion on investigational drugs · 2022Article
- Targeting the succinate receptor effectively inhibits periodontitis.Cell reports · 2022Article
- Article
- Macrophages in Microbial Pathogenesis: Commonalities of Defense Evasion Mechanisms.Infection and immunity · 2022Review
- The Effects ofFrontiers in immunology · 2021Review
- Exercise Promotes the Osteoinduction of HA/β-TCP Biomaterials via the Wnt Signaling Pathway.Metabolites · 2020Article
- Fetal Membrane Inflammation Induces Preterm Birth Via Toll-Like Receptor 2 in Mice With Chronic Gingivitis.Reproductive sciences (Thousand Oaks, Calif.) · 2019Article
- Expression of human and Porphyromonas gingivalis glutaminyl cyclases in periodontitis and rheumatoid arthritis-A pilot study.Archives of oral biology · 2019Article
- Cytosolic DNA Sensing Promotes Macrophage Transformation and Governs Myocardial Ischemic Injury.Circulation · 2018Article
- Oral Biofilms from Symbiotic to Pathogenic Interactions and Associated Disease -Connection of Periodontitis and Rheumatic Arthritis by Peptidylarginine Deiminase.Frontiers in microbiology · 2018Review
- Gum-on-a-Chip Exploring Host-Microbe Interactions: Periodontal Disease Modeling and Drug Discovery.Journal of tissue engineeringArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontal disease is a prevalent chronic inflammatory condition characterised by an aberrant host response to a pathogenic plaque biofilm resulting in local tissue damage and frustrated healing that can result in tooth loss. Cysteine proteases (gingipains) from the key periodontal pathogen Porphyromonas gingivalis have been implicated in periodontal disease pathogenesis by inhibiting inflammation resolution and are linked with systemic chronic inflammatory conditions such as rheumatoid arthritis. Efficient clearance of apoptotic cells is essential for the resolution of inflammation and tissue restoration. Here we sought to characterise the innate immune clearance of apoptotic cells and its modulation by gingipains. We examined the capacity of gingipain-treated macrophages to migrate towards and phagocytose apoptotic cells. Lysine gingipain treatment of macrophages impaired macrophage migration towards apoptotic neutrophils. Furthermore, lysine gingipain treatment reduced surface expression levels of CD14, a key macrophage receptor for apoptotic cells, which resulted in reduced macrophage interactions with apoptotic cells. Additionally, while apoptotic cells and their derived secretome were shown to inhibit TNF-α-induced expression by P. gingivalis lipopolysaccharide, we demonstrated that gingipain preparations induced a rapid inflammatory response in macrophages that was resistant to the anti-inflammatory effects of apoptotic cells or their secretome. Taken together, these data indicate that P. gingivalis may promote the chronic inflammation seen in periodontal disease patients by multiple mechanisms, including rapid, potent gingipain-mediated inflammation, coupled with receptor cleavage leading to defective clearance of apoptotic cells and reduced anti-inflammatory responses. Thus, gingipains represent a potential therapeutic target for intervention in the management of chronic periodontal disease.
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