Research Paper Volume 15, Issue 14 pp 6721—6735

Th1 promotes M1 polarization of intestinal macrophages to regulate colitis-related mucosal barrier damage

Shuiliang Ruan1, *, , Liang Xu2, *, , Yongjia Sheng1, , Jin Wang1, , Xiaohong Zhou1, , Caiqun Zhang1, , Li Guo1, , Wenyan Li1, &, , Chenyang Han1, &, ,

  • 1 The Second Affiliated Hospital of Jiaxing University, Jiaxing 314001, Zhejiang, China
  • 2 Jiaxing University Master Degree Cultivation Base, Zhejiang Chinese Medical University, Hangzhou 310000, Zhejiang, China
* Co-first author

Received: January 15, 2023       Accepted: March 6, 2023       Published: April 4, 2023
How to Cite

Copyright: © 2023 Ruan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


This work aimed to investigate the role of helper T cell 1 (Th1) in chronic colitis and its immunoregulatory mechanism.

The proportions of Th1 and Th2, and the levels of related cytokines in tissues from patients with inflammatory bowel disease (IBD; ulcerative colitis+Crohn's disease, UC+CD) were detected. DSS was used to induce the mouse model of IBD; thereafter, Th1 cells were induced in vitro and amplified before they were injected intraperitoneally. Later, the changes in life state and body weight of mice were observed, the proportion of M1 macrophages in mucosal tissues and mucosal barrier damage were detected. After treatment with macrophage scavenging agent (Clodronate Liposomes, CLL), the influence of Th1 on IBD mice was observed. Then, the intestinal macrophages were co-cultured with Th1 in vitro to observe the influence of Th1 on the polarization of intestinal macrophages. Besides, cells were treated with the STAT3 inhibitor to further detect the macrophage polarization level. Intestinal macrophages were later co-cultured with intestinal epithelial cells to observe the degree of epithelial cell injury.

The Th1 proportions in intestinal tissues of UC and CD patients were higher than those in healthy subjects, but the difference in Th2 proportion was not significant. In the IBD mouse model, Th1 induced the M1 polarization of macrophages, aggravated the intestinal inflammatory response, and resulted in the increased mucosal barrier permeability. Pretreatment with CLL antagonized the effect of Th1 cells, reduced the intestinal tissue inflammatory response and mucosal barrier permeability.


Th1: helper T cell 1; IBD: inflammatory bowel disease; UC: ulcerative colitis; CD: Crohn’s disease; DSS: Dextran Sulfate Sodium Salt; CLL: Clodronate Liposomes; IFN-γ: interferon-γ; TNF-α: tumor necrosis factor-α; NK: natural killer; ELISA: enzyme linked immunosorbent assay; IHC: Immunohistochemical; TJ: tight junction; FCM: Flow Cytometry; TEM: transmission electron microscope; TEER: transepithelial electrical resistance.