Evidence map›Paper›PMID 15538982›Full record

ArticleCurrent infectious disease reports2004

Vaginal Immunity in Bacterial Vaginosis.

Sabina Cauci

Abstract read
PubMed Publisher
In one paragraph

Article in Current infectious disease reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 3 pooled it
2.6field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 3 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Engineered Tissue Models to Decode Host-Microbiota Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  7. Frontiers in cellular and infection microbiology · 2025
    Article
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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

1 author at 1 institution in 1 country.

Sabina CauciDepartment of Biomedical Sciences and Technologies, School of Medicine, University of Udine, Piazzale Kolbe 4, 33100 Udine, Italy. scauci@mail.dstb.uniud.it.
University of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vaginal immunity in response to microbial perturbation is still poorly understood and may be crucial for protection from adverse outcomes associated with bacterial vaginosis (BV). BV is the most prevalent vaginal disorder in adult women worldwide. However, its pathogenesis is still elusive. In BV-positive women, inflammatory signs are scant--approximately 50% of women are asymptomatic. The number of vaginal neutrophils in the BV-positive patient is not increased with respect to healthy women. In contrast, vaginal interleukin (IL)-1beta levels are largely increased. Recent findings indicate that microbial hydrolytic enzymes could be responsible for dampening the expected proinflammatory response cascade after IL-1beta increase. In other words, BV causes a large increase of vaginal IL-1beta, which is not paralleled by an increase of IL-8 levels, suggesting that BV-associated factors specifically dampen IL-8. The impairment of IL-8 increase may explain the absence of neutrophil increase in most women exposed to a massive abnormal anaerobic vaginal colonization (BV). Among BV-positive women, vaginal innate immunity is strongly correlated to a specific adaptive immune response: the immunoglobulin A (IgA) against the hemolysin produced by Gardnerella vaginalis (anti-Gvh IgA), which is the main bacterium present in BV. High anti-Gvh IgA levels are protective for adverse pregnancy outcomes. However, an exaggerated inflammatory response, mainly attributed to genetic polymorphisms, is also implicated in BV-associated adverse outcomes.

Identifiers

PMID15538982
OpenAlexW1976678129

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.