Related Experiment Video
Updated: Jan 14, 2026

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
Published on: December 16, 2021
Indole propionic acid modulates macrophage polarization via TGF-β1/smads to enhance E-cadherin expression in
Qinyuan Yang1, Huaiqin Zhong2, Zhen Zhu3
1Department of Gastroenterology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, China; Department of Geriatrics, Shanghai Health and Medical Center, Wuxi, Jiangsu, 214000, China.
Objectives:
This study investigated the regulatory effects of Indole Propionic Acid (IPA) on macrophage polarization and its role in promoting epithelial integrity via the transforming growth factor-β1 (TGF-β1)/Smads signaling pathway in inflammatory bowel disease (IBD).
Methods:
Peritoneal macrophages (PEMs) from dextran sulfate sodium (DSS)-induced colitis mice, RAW264.7 cells, and bone marrow-derived macrophages (BMDMs) were used to assess IPA's impact on macrophage polarization. Classical (M1) polarization was induced with lipopolysaccharide (LPS), followed by IPA treatment. The TGF-β1/Smads pathway was modulated using SB-431542 or TGF-β1. HCT116 human epithelial cells were co-cultured with PEMs, and epithelial cadherin (E-cadherin) expression was evaluated via histopathology, immunofluorescence, qRT-PCR, and Western blotting. DSS-induced colitis mice received IPA, and colonic tissues were assessed for inflammation, polarization, E-cadherin expression, barrier integrity, and apoptosis.
Results:
IPA suppressed M1 and promoted alternatively activated M2 macrophages (P < 0.05), alleviated inflammation, decreased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), and improved barrier integrity (P < 0.05). Enhanced E-cadherin expression was observed in both IPA-treated mice and HCT116 cells, indicating consistent epithelial protection. IPA inhibited TGF-β1/Smads signaling and reduced epithelial apoptosis. Co-cultures confirmed IPA enhanced proliferation and suppressed apoptosis via TGF-β1/Smads inhibition.
Conclusion:
IPA promotes anti-inflammatory macrophage polarization and enhances epithelial integrity by inhibiting the TGF-β1/Smads pathway, suggesting therapeutic potential in IBD.
More Related Videos
08:37Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
06:57Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells
Published on: September 18, 2016
Related Concept Videos
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
Renewal of Intestinal Stem Cells
Inflammatory Bowel Disease IV: Pharmacological Management
Pharmacologic...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Inflammatory Bowel Disease II: Crohn's Disease
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by...
Inflammatory Bowel Disease I: Ulcerative Colitis
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...