Evidence map›Paper›PMID 31614422›Full record

ArticleInternational journal of molecular sciences2019

Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma.

Ewelina Russjan, Katarzyna Kaczyńska

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The Role of Peptides in Asthma-Obesity Phenotype.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Regulatory Peptides in Asthma.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Peptides for Health Benefits 2019.International journal of molecular sciences · 2020
    Article
  10. Review
  11. 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

2 authors at 1 institution in 1 country.

Ewelina RussjanDepartment of Respiration Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawińskiego Street, 02-106 Warsaw, Poland. erussjan@imdik.pan.pl.
Katarzyna KaczyńskaDepartment of Respiration Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawińskiego Street, 02-106 Warsaw, Poland. kkaczynska@imdik.pan.pl.ORCID 0000-0001-9608-4736
Mossakowski Medical Research Institute, Polish Academy of Sciences · PL

Funding

National Science Centre, Poland 2014/13/B/NZ7/02247
6 · The paper itself

Abstract

Neurotensin (NT) demonstrates ambiguous activity on inflammatory processes. The present study was undertaken to test the potential anti-inflammatory activity of NT in a murine model of non-atopic asthma and to establish the contribution of NTR1 receptors. Asthma was induced in BALB/c mice by skin sensitization with dinitrofluorobenzene followed by intratracheal hapten provocation. The mice were treated intraperitoneally with NT, SR 142948 (NTR1 receptor antagonist) + NT or NaCl. Twenty-four hours after the challenge, airway responsiveness to nebulized methacholine was measured. Bronchoalveolar lavage fluid (BALF) and lungs were collected for biochemical and immunohistological analysis. NT alleviated airway hyperreactivity and reduced the number of inflammatory cells in BALF. These beneficial effects were inhibited by pretreatment with the NTR1 antagonist. Additionally, NT reduced levels of IL-13 and TNF-α in BALF and IL-17A, IL12p40, RANTES, mouse mast cell protease and malondialdehyde in lung homogenates. SR 142948 reverted only a post-NT TNF-α decrease. NT exhibited anti-inflammatory activity in the hapten-induced asthma. Reduced leukocyte accumulation and airway hyperresponsiveness indicate that this beneficial NT action is mediated through NTR1 receptors. A lack of effect by the NTR1 blockade on mast cell activation, oxidative stress marker and pro-inflammatory cytokine production suggests that other pathways can be involved, which requires further research.

Indexed as

AnimalsAnti-Inflammatory AgentsAsthmaBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalGene Expression RegulationHaptensHumansInjections, IntraperitonealLeukocytesMaleMethacholine ChlorideMiceMice, Inbred BALB CNeurotensinAnti-Inflammatory AgentsCytokinesHaptensMethacholine ChlorideNeurotensinPyrazolesQuinolinesSR 142948asthmainflammationneurotensin

Identifiers

PMID31614422
PMCPMC6834300
OpenAlexW2979632148

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.