ArticleScientific reports2023
Depletion of muscularis macrophages ameliorates inflammation-driven dysmotility in murine colitis model.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Sacral Neural Crest-Derived Extracellular Vesicles Promote Pelvic Ganglion Repair Through Anti-Pyroptotic Effects Involving ANXA1-FPR2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- DSS Colitis Model: Traps, Tricks, and Reporting Recommendations.Biomedicines · 2026Review
- Histochemical characterization of muscularis macrophage loss and disruption of a miR-93-5p-AHNAK neuro-immune axis in Hirschsprung's disease.Histochemistry and cell biology · 2026Article
- Heterogeneity of Muscularis Macrophages in the Stomach.Gastro hep advances · 2026Article
- Oral Delivery of Astaxanthin via Carboxymethyl Chitosan-Modified Nanoparticles for Ulcerative Colitis Treatment.Molecules (Basel, Switzerland) · 2024Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Previously, the presence of a blood-myenteric plexus barrier and its disruption was reported in experimentally induced colitis via a macrophage-dependent process. The aim of this study is to reveal how myenteric barrier disruption and subsequent neuronal injury affects gut motility in vivo in a murine colitis model. We induced colitis with dextran sulfate sodium (DSS), with the co-administration of liposome-encapsulated clodronate (L-clodronate) to simultaneously deplete blood monocytes contributing to macrophage infiltration in the inflamed muscularis of experimental mice. DSS-treated animals receiving concurrent L-clodronate injection showed significantly decreased blood monocyte numbers and colon muscularis macrophage (MM) density compared to DSS-treated control (DSS-vehicle). DSS-clodronate-treated mice exhibited significantly slower whole gut transit time than DSS-vehicle-treated animals and comparable to that of controls. Experiments with oral gavage-fed Evans-blue dye showed similar whole gut transit times in DSS-clodronate-treated mice as in control animals. Furthermore, qPCR-analysis and immunofluorescence on colon muscularis samples revealed that factors associated with neuroinflammation and neurodegeneration, including Bax1, Hdac4, IL-18, Casp8 and Hif1a are overexpressed after DSS-treatment, but not in the case of concurrent L-clodronate administration. Our findings highlight that MM-infiltration in the muscularis layer is responsible for colitis-associated dysmotility and enteric neuronal dysfunction along with the release of mediators associated with neurodegeneration in a murine experimental model.
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Registered trials
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