Evidence map›Paper›PMID 21825059›Full record

ArticleInfection and immunity2011

Enhanced neutrophil longevity and recruitment contribute to the severity of oviduct pathology during Chlamydia muridarum infection.

Lauren C Frazer, Catherine M O'Connell, Charles W Andrews, Matthew A Zurenski, Toni Darville

Open access · bronzeAbstract read
In one paragraph

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Pathogenic and Protective Roles of Neutrophils inPathogens (Basel, Switzerland) · 2025
    Review
  6. Article
  7. Article
  8. Microbes and the fate of neutrophils.Immunological reviews · 2023
    Review
  9. Plasmid-mediated virulence inFrontiers in cellular and infection microbiology · 2023
    Review
  10. Genetic susceptibility loci forFrontiers in immunology · 2022
    Article
  11. Article
  12. MiR-378b ModulatesPathogens (Basel, Switzerland) · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Clear Victory forFrontiers in microbiology · 2019
    Review
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Lauren C FrazerChildren's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15224, USA.
Catherine M O'Connell
Charles W Andrews
Matthew A Zurenski
Toni Darville
Children's Hospital of Pittsburgh · USUniversity of Pittsburgh · US

Funding

The UPMC Sexually Transmitted Infections Cooperative Research CenterU19AI084024 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WIESENFELD, HAROLD C · 2009 to 2013
$12.9M
Cell Death and Innate Immunity in Chlamydial InfectionR01AI054624 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DARVILLE, TONI · 2003 to 2014
$3.2M
NIAID NIH HHS R01 AI054624NIAID NIH HHS U19 AI084024
6 · The paper itself

Abstract

Our previous studies revealed that intravaginal infection of mice with a plasmid-deficient strain of Chlamydia muridarum, CM3.1, does not induce the development of oviduct pathology. In this study, we determined that infection with CM3.1 resulted in a significantly reduced frequency and absolute number of neutrophils in the oviducts during acute infection. This reduction in neutrophils was associated with significantly lower levels of neutrophil chemokines in the oviducts and decreased production of neutrophil chemokines by oviduct epithelial cells infected with CM3.1 in vitro. Infection with CM3.1 also resulted in an increased frequency of late apoptotic/dead neutrophils in the oviduct. Examination of the ability of Chlamydia trachomatis to prevent neutrophil apoptosis in vitro revealed that C. trachomatis strain D/UW-3/Cx exhibited an enhanced ability to prevent neutrophil apoptosis compared to plasmid-deficient CTD153, and this effect was dependent on the presence of CD14(high) monocytes. The presence of monocytes also resulted in enhanced neutrophil cytokine production and increased production of tissue-damaging molecules in response to D/UW-3/Cx relative to results with CTD153. Attempts to use antibody-mediated depletion to discern the specific role of neutrophils in infection control and pathology in vivo revealed that although Ly6G(high) neutrophils were eliminated from the blood and oviducts with this treatment, immature neutrophils and high levels of tissue-damaging molecules were still detectable in the upper genital tract. These data support the role of neutrophils in chlamydia-induced pathology and reveal that novel methods of depletion must be developed before their role can be specifically determined in vivo.

Indexed as

AnimalsChlamydia InfectionsChlamydia muridarumFemaleGenital Diseases, FemaleMiceMice, Inbred C3HMice, Inbred C57BLNeutrophil InfiltrationNeutrophilsOviductsSeverity of Illness Index

Identifiers

PMID21825059
PMCPMC3187238
OpenAlexW2105282111

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.