Evidence map›Paper›PMID 19439727›Full record

ReviewBiology of reproduction2009

Defining postpartum uterine disease and the mechanisms of infection and immunity in the female reproductive tract in cattle.

I Martin Sheldon, James Cronin, Leopold Goetze, Gaetano Donofrio, Hans-Joachim Schuberth

Open access · bronzeAbstract readReview
In one paragraph

Review in Biology of reproduction, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
272citing papers in PubMed, 2 pooled it
44.8field-weighted citation impact, top 1% 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

272 citing papers in PubMed, 2 syntheses or guidelines pooled it, 946 citations in OpenAlex.

  1. Pooled it
  2. Recent Advances in Camel Immunology.Frontiers in immunology · 2020
    Pooled it
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  6. The Puerperium in the Modern Dairy Cow: A Review.Reproduction in domestic animals = Zuchthygiene · 2026
    Review
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212 more citing papers are in PubMed but not listed here.

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 4 institutions in 6 countries.

I Martin SheldonInstitute of Life Science, School of Medicine, Swansea University, Swansea, UK. I.M.Sheldon@swansea.ac.uk
James Cronin
Leopold Goetze
Gaetano Donofrio
Hans-Joachim Schuberth
Swansea University · GBDepartment of Animal Health · VNUniversity of Parma · ITUniversity of Veterinary Medicine Hannover, Foundation · DE

Funding

Biotechnology and Biological Sciences Research Council BB/D02028X/1Biotechnology and Biological Sciences Research Council BB/F005121/1Biotechnology and Biological Sciences Research Council BBF0051211
6 · The paper itself

Abstract

Uterine microbial disease affects half of all dairy cattle after parturition, causing infertility by disrupting uterine and ovarian function. Infection with Escherichia coli, Arcanobacterium pyogenes, and bovine herpesvirus 4 causes endometrial tissue damage. Toll-like receptors on endometrial cells detect pathogen-associated molecules such as bacterial DNA, lipids, and lipopolysaccharide (LPS), leading to secretion of cytokines, chemokines, and antimicrobial peptides. Chemokines attract neutrophils and macrophages to eliminate the bacteria, although persistence of neutrophils is associated with subclinical endometritis and infertility. Cows with uterine infections are less likely to ovulate because they have slower growth of the postpartum dominant follicle in the ovary, lower peripheral plasma estradiol concentrations, and perturbation of hypothalamic and pituitary function. The follicular fluid of animals with endometritis contains LPS, which is detected by the TLR4/CD14/LY96 (MD2) receptor complex on granulosa cells, leading to lower aromatase expression and reduced estradiol secretion. If cows with uterine disease ovulate, the peripheral plasma concentrations of progesterone are lower than those in normal animals. However, luteal phases are often extended in animals with uterine disease, probably because infection switches the endometrial epithelial secretion of prostaglandins from the F series to the E series by a phospholipase A2-mediated mechanism, which would disrupt luteolysis. The regulation of endometrial immunity depends on steroid hormones, somatotrophins, and local regulatory proteins. Advances in knowledge about infection and immunity in the female genital tract should be exploited to develop new therapeutics for uterine disease.

Indexed as

AnimalsCattleFemaleImmunityInfectionsPostpartum PeriodUterine DiseasesUterus

Identifiers

PMID19439727
PMCPMC2784443
OpenAlexW2147412811

What OpenQuestion holds

Textmetadata
LicenceTDM
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.