ArticleGastro hep advances2026
Macrophage Immune-Competent Colon Assembloids for Functional Interrogation of Neuroinflammation-Induced Colonic Dysmotility.
Article in Gastro hep advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- EMMIs: Engineered Myometrial Microtissues for Direct Quantification of Oxytocin-Induced Contractility.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Background and Aims: Background and Aims: Functional gastrointestinal disorders affect ∼40% of the global population and are frequently characterized by colonic dysmotility. Symptomatic manifestations of colonic dysmotility significantly reduce quality of life in inflammatory bowel disease, diabetes, and Gulf War Illness. Current in vitro models lack the integration of functional physiology with immune and neuronal complexity required to establish causal links between neuroinflammation and dysmotility. Here, an immune-competent bioengineered colon assembloid is introduced that integrates multiple cell types of the external colonic wall, along with functional readouts of motility. Methods: Bioengineered colon assembloids were fabricated using immortalized smooth muscle cells, enteric neuronal progenitor cells, and macrophage immune cells embedded within collagen hydrogels. Assembloids were allowed to compact and mature, prior to inflammatory insult with pyridostigmine bromide or tumor necrosis factor-alpha. Results: Within bioengineered colon assembloids, various inflammatory insults resulted in enteric neuroinflammation, cascading to changes in colonic motility. Key mechanisms of dysmotility following inflammatory insult within the bioengineered colon assembloids included impaired neuronal regeneration and aberrant smooth muscle remodeling. The bioengineered colon assembloid model mimicked diverse aspects of enteric neuroinflammation. Conclusion: Ultimately, the platform offers a physiologically relevant avenue to interrogate neuroimmune crosstalk and dissect mechanisms of colonic dysmotility, paving the way to new therapeutic strategies to improve colonic motility.
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