Evidence map›Paper›PMID 38139072›Full record

ArticleInternational journal of molecular sciences2023

PEPITEM Treatment Ameliorates EAE in Mice by Reducing CNS Inflammation, Leukocyte Infiltration, Demyelination, and Proinflammatory Cytokine Production.

Mohammed Alassiri, Fahd Al Sufiani, Mohammed Aljohi, Asma Alanazi, Aiman Saud Alhazmi, Bahauddeen M Alrfaei, Hasan Alnakhli, Yasser A Alshawakir, Saleh M Alharby, Abdullah Y Almubarak and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

13 authors at 5 institutions in 1 country.

Mohammed AlassiriDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Center (KAIMRC), Riyadh 11481, Saudi Arabia.ORCID 0000-0001-9830-0551
Fahd Al SufianiDepartment of Pathology and Laboratory Medicine, King Abdulaziz Medical City (KAMC), Ministry of National Guard-Health Affairs (MNGHA), Riyadh 11481, Saudi Arabia.ORCID 0000-0001-9287-1353
Mohammed AljohiHealthy Aging Research Institute, King Abdulaziz City for Science and Technology (KACST), Riyadh 11442, Saudi Arabia.
Asma AlanaziDepartment of Basic Medical Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Center (KAIMRC), King Abdulaziz Medical City (KAMC), Riyadh 11481, Saudi Arabia.
Aiman Saud AlhazmiDepartment of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Center (KAIMRC), Riyadh 11481, Saudi Arabia.
Bahauddeen M AlrfaeiDepartment of Basic Medical Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Center (KAIMRC), King Abdulaziz Medical City (KAMC), Riyadh 11481, Saudi Arabia.ORCID 0000-0002-5740-9187
Hasan AlnakhliDepartment of Pathology and Laboratory Medicine, King Abdulaziz Medical City (KAMC), Ministry of National Guard-Health Affairs (MNGHA), Riyadh 11481, Saudi Arabia.
Yasser A AlshawakirDepartment of Experimental Surgery and Animal Laboratory, College of Medicine, King Saud University, Riyadh 12372, Saudi Arabia.
Saleh M AlharbyDepartment of Experimental Surgery and Animal Laboratory, College of Medicine, King Saud University, Riyadh 12372, Saudi Arabia.
Abdullah Y AlmubarakDepartment of Experimental Surgery and Animal Laboratory, College of Medicine, King Saud University, Riyadh 12372, Saudi Arabia.ORCID 0000-0003-0384-4842
Mohammed AlasseiriDepartment of Medical Laboratory Technology, Faculty of Applied Medical Sciences, University of Tabuk, Tabuk 47512, Saudi Arabia.ORCID 0000-0003-0406-1524
Nora AlorfHealthy Aging Research Institute, King Abdulaziz City for Science and Technology (KACST), Riyadh 11442, Saudi Arabia.
Mashan L AbdullahDepartment of Experimental Medicine, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Center (KAIMRC), Ministry of National Guard-Health Affairs (MNGHA), Riyadh 11481, Saudi Arabia.ORCID 0000-0002-4628-1536
King Saud bin Abdulaziz University for Health Sciences · SAKing Saud University · SAKing Abdulaziz City for Science and Technology · SAKing Abdulaziz Medical City · SAUniversity of Tabuk · SA

Funding

King Abdullah International Medical Research Center RC19/084/R
6 · The paper itself

Abstract

To investigate the effect of the therapeutic treatment of the immunopeptide, peptide inhibitor of trans-endothelial migration (PEPITEM) on the severity of disease in a mouse model of experimental autoimmune encephalomyelitis (EAE) as a model for human multiple sclerosis (MS), a series of experiments were conducted. Using C57BL/6 female mice, we dosed the PEPITEM in the EAE model via IP after observing the first sign of inflammation. The disease was induced using MOG35-55 and complete Freund's adjuvants augmented with pertussis toxin. The EAE score was recorded daily until the end of the experiment (21 days). The histological and immunohistochemistry analysis was conducted on the spinal cord sections. A Western blot analysis was performed to measure the protein concentration of MBP, MAP-2, and N-Cadherin, and ELISA kits were used to measure IL-17 and FOXP3 in the serum and spinal cord lysate. The therapeutic treatment with PEPITEM reduced the CNS infiltration of T cells, and decreased levels of the protein concertations of MBP, MAP-2, and N-Cadherin were observed, in addition to reduced concertations of IL-17 and FOXP3. Using PEPITEM alleviated the severity of the symptoms in the EAE model. Our study revealed the potential of PEPITEM to control inflammation in MS patients and to reduce the harmful effects of synthetic drugs.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsCadherinsCytokinesFemaleForkhead Transcription FactorsHumansInflammationInterleukin-17MiceMice, Inbred C57BLPeptidesSpinal CordT-LymphocytesCadherinsCytokinesForkhead Transcription FactorsInterleukin-17PeptidesdemyelinationEAE modelleukocyte traffickingmultiple sclerosisPEPITEM

Identifiers

PMID38139072
PMCPMC10743148
OpenAlexW4389482634

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.