Evidence map›Paper›PMID 31340824›Full record

ArticleBMC veterinary research2019

Effect of female sex hormones on the developmental cycle of Chlamydia abortus compared to a penicillin-induced model of persistent infection.

D Álvarez, M R Caro, A J Buendía, C Schnee, N Ortega, A Murcia-Belmonte, J Salinas

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC veterinary research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Detection ofJournal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2023
    Article
  3. Review
  4. 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

7 authors at 2 institutions in 2 countries.

D ÁlvarezDepartamento de Sanidad Animal, Facultad de Veterinaria. Campus de Espinardo, Universidad de Murcia, 30100, Murcia, Spain.
M R CaroDepartamento de Sanidad Animal, Facultad de Veterinaria. Campus de Espinardo, Universidad de Murcia, 30100, Murcia, Spain. mrcaro@um.es.
A J BuendíaDepartamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Regional Campus of International Excellence 'Campus Mare Nostrum, Universidad de Murcia, Murcia, Spain.
C SchneeFriedrich-Loeffler-Institut, Institute of Molecular Pathogenesis, Jena, Germany.
N OrtegaDepartamento de Sanidad Animal, Facultad de Veterinaria. Campus de Espinardo, Universidad de Murcia, 30100, Murcia, Spain.
A Murcia-BelmonteDepartamento de Sanidad Animal, Facultad de Veterinaria. Campus de Espinardo, Universidad de Murcia, 30100, Murcia, Spain.
J SalinasDepartamento de Sanidad Animal, Facultad de Veterinaria. Campus de Espinardo, Universidad de Murcia, 30100, Murcia, Spain.
Universidad de Murcia · ESFriedrich-Loeffler-Institut · DE

Funding

Ministerio de Economía, Industria y Competitividad, Gobierno de España Grant AGL2013-45868-R
6 · The paper itself

Abstract

backgroundChlamydia abortus, an obligate intracellular pathogen with an affinity for placenta, causes reproductive failure. In non-pregnant animals, an initial latent infection is established until the next gestation, when the microorganism is reactivated, causing abortion. The precise mechanisms that trigger the awakening of C. abortus are still unknown. Sexual hormones such as estradiol and progesterone have been shown to affect the outcome of infection in other species of the family Chlamydiaceae, while estrogens increase chlamydial infection, progesterone has the opposite effect. To try to establish whether there is a relationship between these events and the latency/ reactivation of C. abortus in the reproductive tract of small ruminants, ovine endometrial (LE) and trophoblastic (AH-1) cells were treated with estradiol or progesterone prior to their infection with C. abortus. The results are compared with those obtained for treatment with penicillin prior to infection, which is a well-established model for studying persistent infection in other chlamydial species. Cells were examined by transmission electron microscopy, and an mRNA expression analysis of 16 genes related to the chlamydial developmental cycle was made.

resultsThe changes observed in this study by the action of sex hormones seem to depend on the type of cell where the infection develops. In addition, while the changes are morphologically similar to those induced by treatment with penicillin, the patterns of gene expression are different. Gene expression patterns therefore, seem to depend on the persistence induced models of C. abortus used. Hormone treatments induced aberrant forms in infected endometrial cells but did not affect the chlamydial morphology in trophoblast cells. At the genetic level, hormones did not induce significant changes in the expression of the studied genes.

conclusionsThe results suggest that penicillin induces a state of persistence in in vitro cultured C. abortus with characteristic morphological features and gene transcriptional patterns. However, the influence of hormones on the C. abortus developmental cycle is mediated by changes in the host cell environment. Furthermore, a persistent state in C. abortus cannot be characterised by a single profile of gene expression pattern, but may change depending on the model used to induce persistence.

Indexed as

AnimalsCell LineChlamydiaChlamydia InfectionsEstradiolFemaleGene ExpressionMicroscopy, Electron, TransmissionPenicillinsProgesteroneRNA, MessengerSheepEstradiolPenicillinsProgesteroneRNA, MessengerChlamydia abortusFemale sex hormonesOvine enzootic abortionPenicillinPersistence

Identifiers

PMID31340824
PMCPMC6657046
OpenAlexW2963072657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.