Evidence map›Paper›PMID 28802412›Full record

ArticleTuberculosis (Edinburgh, Scotland)2017

Mycobacterium tuberculosis sigE mutant ST28 used as a vaccine induces protective immunity in the guinea pig model.

JoLynn Troudt, Elizabeth Creissen, Linda Izzo, Helle Bielefeldt-Ohmann, Stefano Casonato, Riccardo Manganelli, Angelo A Izzo

Abstract read
In one paragraph

Article in Tuberculosis (Edinburgh, Scotland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Structure of the SigE regulatory network inFrontiers in microbiology · 2024
    Article
  2. Review
  3. SigE: A master regulator ofFrontiers in microbiology · 2023
    Review
  4. Review
  5. Review
  6. Article
  7. Review
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.

JoLynn TroudtColorado State University, Department of Microbiology, Immunology & Pathology, 1682 Campus Delivery, Fort Collins, CO, 80523, USA.
Elizabeth CreissenColorado State University, Department of Microbiology, Immunology & Pathology, 1682 Campus Delivery, Fort Collins, CO, 80523, USA.
Linda IzzoColorado State University, Department of Microbiology, Immunology & Pathology, 1682 Campus Delivery, Fort Collins, CO, 80523, USA.
Helle Bielefeldt-OhmannUniversity of Queensland, Australian Infectious Diseases Research Centre, St. Lucia, Qld, 4072 & School of Veterinary Science, Gatton Campus, Qld, 4343, Australia.
Stefano CasonatoUniversity of Padova, Department Molecular Medicine, Via Gabelli 63, 35121, Padova, Italy.
Riccardo ManganelliUniversity of Padova, Department Molecular Medicine, Via Gabelli 63, 35121, Padova, Italy.
Angelo A IzzoColorado State University, Department of Microbiology, Immunology & Pathology, 1682 Campus Delivery, Fort Collins, CO, 80523, USA. Electronic address: angelo.izzo@colostate.edu.

Funding

NIAID NIH HHS HHSN272201000009I
6 · The paper itself

Abstract

With more than 9 million new infections and 1.5 million deaths claimed every year, tuberculosis remains one of the major scourges of humankind. The only vaccine available against this disease, the attenuated strain Mycobacterium bovis, BCG is effective against severe forms of the disease in infants, but scarcely effective in protecting adults from the pulmonary form of the disease, thus not stopping transmission. Consequently, the development of an effective anti-tuberculosis vaccine is a major goal for improving global health. The most common concept is that a more effective vaccine should include a first immunization with a live vaccine followed by the administration of an acellular boosting vaccine. In this approach, the live vaccine might be either BCG or a different, more efficient attenuated strain. Recently, we showed that a Mycobacterium tuberculosis mutant missing the gene encoding for the extracellular function sigma factor SigE, is strongly attenuated and is able to induce a more effective protection from M. tuberculosis infection compared to BCG in mice. We now further characterize the protective potential of this novel strain in the guinea pig model of tuberculosis. In the guinea pig, it had limited growth but induced a Th1 immune response and was able to significantly reduce the number of colony forming units as well as prolong survival. Taken together these data provide evidence for the use of the M. tuberculosis sigE mutant as the basis for further development as a vaccine against infection.

Indexed as

MutationAnimalsBacterial ProteinsCytokinesDisease Models, AnimalGuinea PigsHost-Pathogen InteractionsLungMycobacterium tuberculosisSigma FactorTh1 CellsTime FactorsTuberculosis, PulmonaryTuberculosis VaccinesVaccines, AttenuatedBacterial ProteinsCytokinessigE protein, BacteriaSigma FactorTuberculosis VaccinesVaccines, Attenuated

Identifiers

PMID28802412
PMCPMC5570617

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.