ArticleInfection and immunity2003
Gonococcal phospholipase d modulates the expression and function of complement receptor 3 in primary cervical epithelial cells.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 50 citations in OpenAlex.
- A surface-exposed cardiolipin synthase provides an unexpected paradigm for maintaining the Gram-negative outer membrane.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- Article
- Complement receptor 3 mediatesVirulence · 2021Article
- Comprehensive genome analysis and comparisons of the swine pathogen, Chlamydia suis reveals unique ORFs and candidate host-specificity factors.Pathogens and disease · 2021Article
- Recent advances in understanding and combattingFaculty reviews · 2021Review
- Targeting phospholipase D in cancer, infection and neurodegenerative disorders.Nature reviews. Drug discovery · 2017Review
- Article
- Is gonococcal disease preventable? The importance of understanding immunity and pathogenesis in vaccine development.Critical reviews in microbiology · 2016Review
- Bacterial Sphingomyelinases and Phospholipases as Virulence Factors.Microbiology and molecular biology reviews : MMBR · 2016Review
- Discovery of desketoraloxifene analogues as inhibitors of mammalian, Pseudomonas aeruginosa, and NAPE phospholipase D enzymes.ACS chemical biology · 2015Article
- Biochemical characterization of a Pseudomonas aeruginosa phospholipase D.Biochemistry · 2015Article
- Acinetobacter baumannii Virulence Is Mediated by the Concerted Action of Three Phospholipases D.PloS one · 2015Article
- Genome sequencing and comparative analysis of three Chlamydia pecorum strains associated with different pathogenic outcomes.BMC genomics · 2014Article
- Moraxella catarrhalis expresses a cardiolipin synthase that impacts adherence to human epithelial cells.Journal of bacteriology · 2014Article
- Factor VII and protein C are phosphatidic acid-binding proteins.Biochemistry · 2013Article
- Construction and characterization of a derivative of Neisseria gonorrhoeae strain MS11 devoid of all opa genes.Journal of bacteriology · 2012Article
- Effect of phosphatidylcholine on pld gene expression level of Aspergillus fumigatus by the real time PCR method and investigations of these genes using bioinformatics analysis.Iranian journal of microbiology · 2012Article
- Phospholipase D: enzymology, functionality, and chemical modulation.Chemical reviews · 2011Review
- The Pathobiology of Neisseria gonorrhoeae Lower Female Genital Tract Infection.Frontiers in microbiology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
CR3-mediated endocytosis is a primary mechanism by which Neisseria gonorrhoeae elicits membrane ruffling and cellular invasion of the cervical epithelia. Our data indicate that, upon infection of cervical epithelia, N. gonorrhoeae specifically releases proteins, including a phospholipase D (PLD) homolog, which facilitate membrane ruffling. To elucidate the function of gonococcal PLD in infection of the cervical epithelia, we constructed an N. gonorrhoeae PLD mutant. By comparative association and/or invasion assays, we demonstrated that PLD mutant gonococci are impaired in their ability to adhere to and to invade primary cervical cells. This defect can be rescued by the addition of supernatants obtained from wild-type-infected cell monolayers but not by exogenously added Streptomyces PLD. The decreased level of total cell association (i.e., adherence and invasion) observed for mutant gonococci is, in part, attributed to the inability of these bacteria to recruit CR3 to the cervical cell surface with extended infection. Using electron microscopy, we demonstrate that gonococcal PLD may be necessary to potentiate membrane ruffling and clustering of gonococci on the cervical cell surface. These data may be indicative of the inability of PLD mutant gonococci to recruit CR3 to the cervical cell surface. Alternatively, in the absence of gonococcal PLD, signal transduction events required for CR3 clustering may not be activated. Collectively, our data indicate that PLD augments CR3-mediated gonococcus invasion of and survival within cervical epithelia.
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.