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Updated: Oct 5, 2025

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
Protecting tissue integrity and enteric function: the case for type 2 inflammation and macrophages.
Qihua Ye1, Barbara Balestrieri1, Nora A Barrett1
1Jeff and Penny Vinik Center for Translational Immunology Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA.
Type 2 inflammation (T2I) protects gut neurons and function. Helminth infections promote T2I, expanding Arginase-1 (Arg-1) macrophages to preserve excitatory neurons and enteric function in inflamed tissues.
Area of Science:
- Immunology
- Neuroscience
- Gastroenterology
Background:
- Type 2 inflammation (T2I) is associated with various inflammatory conditions.
- The precise protective mechanisms of T2I in barrier tissues remain incompletely understood.
Purpose of the Study:
- To investigate the role of helminth-elicited Type 2 inflammation in maintaining enteric function.
- To elucidate the cellular mechanisms underlying T2I-mediated neuroprotection in the gut.
Main Methods:
- Utilized a helminth infection model to induce T2I in the gut.
- Analyzed the expansion and function of Arginase-1 (Arg-1)-expressing macrophages.
- Assessed the impact of T2I on excitatory neurons and overall enteric function.
Main Results:
- Helminth-elicited T2I was found to preserve excitatory neurons.
- Expansion of Arginase-1 (Arg-1)-expressing macrophages was a key feature of this T2I.
- This macrophage expansion correlated with preserved enteric function.
Conclusions:
- Type 2 inflammation can orchestrate protective functions in inflamed barrier tissues.
- Arginase-1-expressing macrophages play a critical role in T2I-mediated neuroprotection.
- These findings expand our understanding of T2I's beneficial roles in inflammatory diseases.
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