Evidence map›Paper›PMID 34572117›Full record

ArticleCells2021

An Autophagy Modulator Peptide Prevents Lung Function Decrease and Corrects Established Inflammation in Murine Models of Airway Allergy.

François Daubeuf, Nicolas Schall, Nathalie Petit-Demoulière, Nelly Frossard, Sylviane Muller

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Therapeutic effects of peptide P140 in a mouse periodontitis model.Cellular and molecular life sciences : CMLS · 2022
    Article
  8. Article
  9. Review
  10. The Role of Autophagy in the Function of CD4Frontiers in pharmacology · 2022
    Review
  11. 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 1 institution in 1 country.

François DaubeufCNRS-Strasbourg University Laboratoire d'Innovation Thérapeutique/Strasbourg Drug Discovery and Development Institute (IMS), Faculté de Pharmacie, 67400 Illkirch, France.
Nicolas SchallCNRS-Strasbourg University Unit Biotechnology and Cell Signaling/Strasbourg Drug Discovery and Development Institute (IMS), Ecole Supérieure de Biotechnologie de Strasbourg, 67400 Illkirch, France.
Nathalie Petit-DemoulièreCNRS-Strasbourg University Laboratoire d'Innovation Thérapeutique/Strasbourg Drug Discovery and Development Institute (IMS), Faculté de Pharmacie, 67400 Illkirch, France.
Nelly FrossardCNRS-Strasbourg University Laboratoire d'Innovation Thérapeutique/Strasbourg Drug Discovery and Development Institute (IMS), Faculté de Pharmacie, 67400 Illkirch, France.
Sylviane MullerCNRS-Strasbourg University Unit Biotechnology and Cell Signaling/Strasbourg Drug Discovery and Development Institute (IMS), Ecole Supérieure de Biotechnologie de Strasbourg, 67400 Illkirch, France.ORCID 0000-0002-0481-0620
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The involvement of autophagy and its dysfunction in asthma is still poorly documented. By using a murine model of chronic house dust mite (HDM)-induced airway inflammation, we tested the expression of several autophagy markers in the lung and spleen of asthma-like animals. Compared to control mice, in HDM-sensitized and challenged mice, the expression of sequestosome-1/p62, a multifunctional adaptor protein that plays an important role in the autophagy machinery, was raised in the splenocytes. In contrast, its expression was decreased in the neutrophils recovered from the bronchoalveolar fluid, indicating that autophagy was independently regulated in these two compartments. In a strategy of drug repositioning, we treated allergen-sensitized mice with the therapeutic peptide P140 known to target chaperone-mediated autophagy. A single intravenous administration of P140 in these mice resulted in a significant reduction in airway resistance and elastance, and a reduction in the number of neutrophils and eosinophils present in the bronchoalveolar fluid. It corrected the autophagic alteration without showing any suppressive effect in the production of IgG1 and IgE. Collectively, these findings show that autophagy processes are altered in allergic airway inflammation. This cellular pathway may represent a potential therapeutic target for treating selected patients with asthma.

Indexed as

AnimalsAsthmaAutophagyBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalEosinophilsFemaleHypersensitivityImmunoglobulin EInflammationLungMaleMiceMice, Inbred BALB CPeptide FragmentsCytokinesImmunoglobulin EPeptide FragmentsSequestosome-1 ProteinSqstm1 protein, mouseallergic asthmaautophagymurine modelsneutrophilspeptide-based treatment

Identifiers

PMID34572117
PMCPMC8472429
OpenAlexW3200883958

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.