Evidence map›Paper›PMID 39656240›Full record

ArticleCell and tissue research2025

TNBS colitis induces architectural changes and alpha-synuclein overexpression in mouse distal colon: A morphological study.

Arianna Casini, Giorgio Vivacqua, Ludovica Ceci, Stefano Leone, Rosa Vaccaro, Marco Tagliafierro, Filippo Maria Bassi, Sara Vitale, Emanuele Bocci, Luigi Pannarale and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell and tissue research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Mechanisms and clinical implications of gut-brain interactions.The Journal of clinical investigation · 2026
    Review
  3. Review
  4. 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

19 authors.

Arianna Casini *Department of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Giorgio Vivacqua *Integrated Research Center (PRAAB), Campus Biomedico University of Rome, Rome, Italy.
Ludovica CeciDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Stefano LeoneDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Rosa VaccaroDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Marco TagliafierroDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Filippo Maria BassiDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Sara VitaleDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Emanuele BocciDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Luigi PannaraleDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Simone CarottiIntegrated Research Center (PRAAB), Campus Biomedico University of Rome, Rome, Italy.
Antonio FranchittoDivision of Health Sciences, Department of Movement, Human and Health Sciences, University of Rome Foro Italico, Rome, Italy.
Patrizia ManciniDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Roberta SferraDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Antonella VetuschiDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Giovanni LatellaDivision of Gastroenterology, Hepatology and Nutrition, Department of Life, Health & Environmental Sciences, San Salvatore Hospital, University of L'Aquila, L'Aquila, Italy.
Paolo OnoriDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Eugenio GaudioDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy.
Romina MancinelliDepartment of Anatomical, Histological, Forensic Medicine and Orthopaedics Sciences, Sapienza University of Rome, Via Alfonso Borelli 50 - 00161, Rome, Italy. romina.mancinelli@uniroma1.it.

Funding

Sapienza Università di Roma RM12117A769CB66ASapienza Università di Roma RM12117A7AF3C286
6 · The paper itself

Abstract

Alpha-synuclein (α-syn) is widely expressed in presynaptic neuron terminals, and its structural alterations play an important role in the pathogenesis of Parkinson's disease (PD). Aggregated α-syn has been found in brain, in the peripheral nerves of the enteric nervous system (ENS) and in the intestinal neuroendocrine cells during synucleinopathies and inflammatory bowel disorders. In the present study, we evaluated the histomorphological features of murine colon with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, a common model of colitis. Thereafter, we investigated the expression of α-syn, Toll-like receptor 4 (TLR4), choline acetyltransferase (ChAT), vasoactive intestinal peptide (VIP), tyrosine hydroxylase (TH), calcitonin gene-related peptide (CGRP), and calcitonin-like receptor (CALCR). Finally, we investigated the presence of phosphorylated α-syn (pS129 α-syn) aggregates and their relationship with inflammatory cells. Colon from TNBS mice showed an increase in inflammatory cells infiltrate and significative changes in the architecture of the intestinal mucosa. α-Syn expression was significantly higher in inflamed colon. VIP was increased in both the mucosa and muscularis externa of TNBS mice, while TH, CGRP, and CALCR were significantly reduced in TNBS mice. Amyloid aggregates of pS129 α-syn were detectable in the ENS, as in the macrophages around the glands of the mucosa correlating with the markers of inflammation. This study describes - for the first time - the altered expression of α-syn and the occurrence of amyloid α-syn aggregates in the inflammatory cells under colitis, supporting the critical role of bowel inflammation in synucleinopathies and the involvement of α-syn in IBD.

Indexed as

alpha-SynucleinColitisColonTrinitrobenzenesulfonic AcidAnimalsMaleMiceMice, Inbred C57BLalpha-SynucleinTrinitrobenzenesulfonic AcidAlpha-synucleinColitisEnteric nervous systemGut-brain axisInflammatory bowel disease

Identifiers

PMID39656240
PMCPMC11787265

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.