ArticleMolecular microbiology2022
The emerging oral pathogen, Filifactor alocis, extends the functional lifespan of human neutrophils.
Article in Molecular microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 20 citations in OpenAlex.
- Prevalence ofPathogens (Basel, Switzerland) · 2026Observational
- Article
- Neutrophil activity compromises root caries remineralization and alters caries-affected-like dentin.Clinical oral investigations · 2025Article
- Article
- Article
- The impact of aging on neutrophil functions and the contribution to periodontitis.International journal of oral science · 2025Review
- Bioscaffold materials resist infection and promote bone defect repair by regulating neutrophil function.Frontiers in bioengineering and biotechnology · 2025Review
- Dying for a cause: The pathogenic manipulation of cell death and efferocytic pathways.Molecular oral microbiology · 2024Review
- An update on periodontal inflammation and bone loss.Frontiers in immunology · 2024Review
- Exploring the Role of IL-17A in Oral Dysbiosis-Associated Periodontitis and Its Correlation with Systemic Inflammatory Disease.Dentistry journal · 2023Review
- Whole Genome Sequencing and Phenotypic Analysis of Antibiotic Resistance inAntibiotics (Basel, Switzerland) · 2023Article
- Neutrophils in the periodontium: Interactions with pathogens and roles in tissue homeostasis and inflammation.Immunological reviews · 2023Review
- Article
- Oral Microorganisms and Biofilms: New Insights to Defeat the Main Etiologic Factor of Oral Diseases.Microorganisms · 2022Article
- Extracellular Vesicle Subproteome Differences amongMicroorganisms · 2022Article
- The emerging oral pathogen, Filifactor alocis, extends the functional lifespan of human neutrophils.Molecular microbiology · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Periodontitis is a chronic inflammatory infectious disease that affects the integrity of tooth-supporting tissues and has adverse systemic consequences. Advances in sequencing technologies have uncovered organisms that are exclusively found in high numbers in periodontal lesions, such as the gram-positive anaerobic rod, Filifactor alocis. F. alocis can manipulate neutrophil effector functions, which allows the organism to survive within these granulocytes. Several neutrophil functions have been tested in the context of F. alocis challenge, but the effect of the organism on neutrophil apoptosis is still unknown. RNA sequencing of human neutrophils challenged with F. alocis showed that apoptosis pathways were differentially regulated. Compared to media-cultured controls, F. alocis-challenged neutrophils maintain their nuclear morphology, do not stain for Annexin V or 7-AAD, and have decreased DNA fragmentation. Inhibition of apoptosis by F. alocis involved reduced caspase-3, -8, and - 9 activation and upregulation of important anti-apoptotic proteins. Prolonged lifespan was dependent on contact through TLR2/6, and F. alocis-challenged neutrophils retained their functional capacity to induce inflammation for longer timepoints. This is the first in-depth characterization of neutrophil apoptotic programs in response to an oral pathogen and provides key information on how bacteria manipulate immune cell mechanisms to maintain a dysregulated inflammatory response.
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.