ArticleInfection and immunity2016
Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- Neutrophil Killing ofJournal of innate immunity · 2026Article
- Host- and genotype-specific transcriptomic responses toFrontiers in immunology · 2026Article
- Article
- The impact of aging on neutrophil functions and the contribution to periodontitis.International journal of oral science · 2025Review
- Increased bacterial load ofFrontiers in oral health · 2025Article
- An inflammatory paradox: strategies inflammophilic oral pathobionts employ to exploit innate immunity via neutrophil manipulation.Frontiers in oral health · 2024Article
- Neutrophils in the periodontium: Interactions with pathogens and roles in tissue homeostasis and inflammation.Immunological reviews · 2023Review
- Selenomonas sputigena Interactions with Gingival Epithelial Cells That Promote Inflammation.Infection and immunity · 2023Article
- miRNA-141-5p Affects the Levels of Neutrophil Elastase in Preeclampsia by Regulating MAPK1.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2022Article
- The emerging oral pathogen, Filifactor alocis, extends the functional lifespan of human neutrophils.Molecular microbiology · 2022Article
- The Age-Driven Decline in Neutrophil Function Contributes to the Reduced Efficacy of the Pneumococcal Conjugate Vaccine in Old Hosts.Frontiers in cellular and infection microbiology · 2022Article
- Host and bacterial factors linking periodontitis and rheumatoid arthritis.Frontiers in immunology · 2022Review
- Extracellular vesicles derived from the periodontal pathogen Filifactor alocis induce systemic bone loss through Toll-like receptor 2.Journal of extracellular vesicles · 2021Article
- Understanding the role of neutrophils in acute respiratory distress syndrome.Biomedical journal · 2021Review
- Article
- Polymicrobial communities in periodontal disease: Their quasi-organismal nature and dialogue with the host.Periodontology 2000 · 2021Review
- Periodontal Pathogens' strategies disarm neutrophils to promote dysregulated inflammation.Molecular oral microbiology · 2021Review
- Article
- The Hunger Games:Frontiers in immunology · 2021Article
- Manipulating neutrophil degranulation as a bacterial virulence strategy.PLoS pathogens · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Filifactor alocis is a recently recognized periodontal pathogen; however, little is known regarding its interactions with the immune system. As the first-responder phagocytic cells, neutrophils are recruited in large numbers to the periodontal pocket, where they play a crucial role in the innate defense of the periodontium. Thus, in order to colonize, successful periodontal pathogens must devise means to interfere with neutrophil chemotaxis and activation. In this study, we assessed major neutrophil functions, including degranulation and cell migration, associated with the p38 mitogen-activated protein kinase (MAPK) signaling pathway upon challenge with F. alocis. Under conditions lacking a chemotactic gradient, F. alocis-challenged neutrophils had increased migration compared to uninfected cells, indicating that F. alocis increases chemokinesis in human neutrophils. In addition, neutrophil chemotaxis induced by interleukin-8 was significantly enhanced when cells were challenged with F. alocis, compared to noninfected cells. Similar to live bacteria, heat-killed F. alocis induced both random and directed migration of human neutrophils. The interaction of F. alocis with Toll-like receptor 2 induced granule exocytosis along with a transient ERK1/2 and sustained p38 MAPK activation. Moreover, F. alocis-induced secretory vesicle and specific granule exocytosis were p38 MAPK dependent. Blocking neutrophil degranulation with TAT-SNAP23 fusion protein significantly reduced the chemotactic and random migration induced by F. alocis Therefore, we propose that induction of random migration by F. alocis will prolong neutrophil traffic time in the gingival tissue, and subsequent degranulation will contribute to tissue damage.
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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.