ArticleInfection and immunity2011
Porphyromonas gingivalis-host interactions in a Drosophila melanogaster model.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Porphyromonas gingivalis Virulence Factors and Clinical Significance in Periodontal Disease and Coronary Artery DiseasesPathogens (Basel, Switzerland) · 2022Review
- Gemella haemolysans inhibits the growth of the periodontal pathogen Porphyromonas gingivalis.Scientific reports · 2021Article
- Roles of Porphyromonas gingivalis and its virulence factors in periodontitis.Advances in protein chemistry and structural biology · 2020Review
- Thioester-containing proteins in the tsetse fly (Glossina) and their response to trypanosome infection.Insect molecular biology · 2018Article
- Quorum-sensing regulator RhlR but not its autoinducer RhlI enablesEMBO reports · 2018Article
- The distinct function of Tep2 and Tep6 in the immune defense of Drosophila melanogaster against the pathogen Photorhabdus.Virulence · 2017Article
- Thioester-containing proteins regulate the Toll pathway and play a role in Drosophila defence against microbial pathogens and parasitoid wasps.BMC biology · 2017Article
- Arthropod Innate Immune Systems and Vector-Borne Diseases.Biochemistry · 2017Review
- Evolution and Function of Thioester-Containing Proteins and the Complement System in the Innate Immune Response.Frontiers in immunology · 2017Review
- Thioester-Containing Protein-4 Regulates the Drosophila Immune Signaling and Function against the Pathogen Photorhabdus.Journal of innate immunity · 2017Article
- Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line.Frontiers in microbiology · 2016Review
- The Drosophila melanogaster host model.Journal of oral microbiology · 2012Article
- The capsule of Porphyromonas gingivalis leads to a reduction in the host inflammatory response, evasion of phagocytosis, and increase in virulence.Infection and immunity · 2011Article
- Porphyromonas gingivalis virulence in a Drosophila melanogaster model.Infection and immunity · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Porphyromonas gingivalis is a Gram-negative obligate anaerobe that has been implicated in the etiology of adult periodontitis. We recently introduced a Drosophila melanogaster killing model for examination of P. gingivalis-host interactions. In the current study, the Drosophila killing model was used to characterize the host response to P. gingivalis infection by identifying host components that play a role during infection. Drosophila immune response gene mutants were screened for altered susceptibility to killing by P. gingivalis. The Imd signaling pathway was shown to be important for the survival of Drosophila infected by nonencapsulated P. gingivalis strains but was dispensable for the survival of Drosophila infected by encapsulated P. gingivalis strains. The P. gingivalis capsule was shown to mediate resistance to killing by Drosophila antimicrobial peptides (Imd pathway-regulated cecropinA and drosocin) and human beta-defensin 3. Drosophila thiol-ester protein II (Tep II) and Tep IV and the tumor necrosis factor (TNF) homolog Eiger were also involved in the immune response against P. gingivalis infection, while the scavenger receptors Eater and Croquemort played no roles in the response to P. gingivalis infection. This study demonstrates that the Drosophila killing model is a useful high-throughput model for characterizing the host response to P. gingivalis infection and uncovering novel interactions between the bacterium and the host.
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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.