Evidence map›Paper›PMID 19892865›Full record

ArticleInvestigative ophthalmology & visual science2010

Role of neutrophils, MyD88-mediated neutrophil recruitment, and complement in antibody-mediated defense against Pseudomonas aeruginosa keratitis.

Tanweer S Zaidi, Tauqeer Zaidi, Gerald B Pier

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Microorganisms · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Complement and CD4eLife · 2019
    Article
  14. MyD88 Deficiency Protects Against Dry Eye-Induced Damage.Investigative ophthalmology & visual science · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Role of MyD88 in adenovirus keratitis.Immunology and cell biology · 2017
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Tanweer S ZaidiChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Tauqeer Zaidi
Gerald B Pier
Brigham and Women's Hospital · USHarvard University · US

Funding

Pathogensis of Bacterial corneal infectionR01EY016144 · NEI · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 2005 to 2018
$5.6M
NEI NIH HHS EY016144NEI NIH HHS R01 EY016144
6 · The paper itself

Abstract

Purpose. Ulcerative keratitis due to Pseudomonas aeruginosa is a sight-threatening disease leading to loss of vision due to corneal inflammation. A human IgG1 monoclonal antibody (MAb F429) to the alginate capsule significantly reduces pathology and bacterial burdens in the cornea when applied topically starting 8 hours post-infection. The purpose of this study was to determine whether local polymorphonuclear neutrophils (PMN) recruitment and complement were important lipopolysaccharide co-factors in MAb F429-mediated reductions in P. aeruginosa tissue levels and corneal pathology. Methods. MyD88 knock-out mice unable to recruit PMN to tissues, mice depleted of PMNs, or mice depleted of complement component C3 were topically treated with MAb F429 starting 8 hours post-infection and evaluated for bacterial levels and corneal pathology 48 hours after infection with two P. aeruginosa isolates. Results. An inability to recruit PMN or systemic PMN depletion plus topical application of MAb F429 resulted in less pathology in the eye, but bacterial burdens were markedly increased in the cornea, brains, and spleens of these mice, indicative of systemic spread. Intraperitoneal injection of cobra venom factor (CVF) reduced C3 levels in the cornea approximately 40%, which did not change the beneficial effects of MAb F429. Both systemic injection and topical application of CVF reduced local C3 levels >60%, which eliminated MAb-mediated reductions in corneal pathology and bacterial levels. Conclusions. PMN recruitment and complement are both needed for maximal in vivo efficacy of MAb F429 in therapeutically treating P. aeruginosa keratitis, and attempts to reduce pathology by limiting PMN influx could have consequences leading to more extensive local and systemic infection.

Indexed as

AnimalsAntibodies, BacterialAntibodies, MonoclonalBacterial ProteinsComplement C3Corneal UlcerEye Infections, BacterialGene SilencingImmunoglobulin GMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88Neutrophil InfiltrationAlgK protein, Pseudomonas aeruginosaAntibodies, BacterialAntibodies, MonoclonalBacterial ProteinsComplement C3Immunoglobulin GMyd88 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID19892865
PMCPMC2868398
OpenAlexW2017731201

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.