Evidence map›Paper›PMID 29765355›Full record

ReviewFrontiers in endocrinology2018

Tuberculosis, the Disrupted Immune-Endocrine Response and the Potential Thymic Repercussion As a Contributing Factor to Disease Physiopathology.

Luciano D'Attilio, Natalia Santucci, Bettina Bongiovanni, María L Bay, Oscar Bottasso

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Studies on the contribution of PPAR Gamma to tuberculosis physiopathology.Frontiers in cellular and infection microbiology · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Immune exhaustion in bacterial infections: mechanisms, consequences, and therapeutic implications.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
    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

5 authors at 2 institutions in 1 country.

Luciano D'AttilioInstituto de Inmunología Clínica y Experimental de Rosario, UNR-CONICET, Rosario, Argentina.
Natalia SantucciInstituto de Inmunología Clínica y Experimental de Rosario, UNR-CONICET, Rosario, Argentina.
Bettina BongiovanniInstituto de Inmunología Clínica y Experimental de Rosario, UNR-CONICET, Rosario, Argentina.
María L BayInstituto de Inmunología Clínica y Experimental de Rosario, UNR-CONICET, Rosario, Argentina.
Oscar BottassoInstituto de Inmunología Clínica y Experimental de Rosario, UNR-CONICET, Rosario, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARInstituto de Biología Molecular y Celular de Rosario · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon the pathogen encounter, the host seeks to ensure an adequate inflammatory reaction to combat infection but at the same time tries to prevent collateral damage, through several regulatory mechanisms, like an endocrine response involving the production of adrenal steroid hormones. Our studies show that active tuberculosis (TB) patients present an immune-endocrine imbalance characterized by an impaired cellular immunity together with increased plasma levels of cortisol, pro-inflammatory cytokines, and decreased amounts of dehydroepiandrosterone. Studies in patients undergoing specific treatment revealed that cortisol levels remained increased even after several months of initiating therapy. In addition to the well-known metabolic and immunological effects, glucocorticoids are involved in thymic cortical depletion with immature thymocytes being quite sensitive to such an effect. The thymus is a central lymphoid organ supporting thymocyte T-cell development, i.e., lineage commitment, selection events and thymic emigration. While thymic TB is an infrequent manifestation of the disease, several pieces of experimental and clinical evidence point out that the thymus can be infected by mycobacteria. Beyond this, the thymic microenvironment during TB may be also altered because of the immune-hormonal alterations. The thymus may be then an additional target of organ involvement further contributing to a deficient control of infection and disease immunopathology.

Indexed as

hormonesimmune-endocrine communicationinflammationpathophysiologythymic involutiontuberculosis

Identifiers

PMID29765355
PMCPMC5938357
OpenAlexW2802998825

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.