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Updated: May 8, 2026
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
Tarm1 may affect colitis by regulating macrophage M1 polarization in a mouse colitis model
Kun Zhang1, Lingfen Xu1, Jing Guo2
1Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, PR China.
Background:
In this study, we aimed to explore the role of Tarm1 in juvenile mice with dextran sulfate sodium (DSS)-induced colitis and elucidate the mechanisms that affect intestinal barrier function.
Methods:
A DSS-induced pediatric inflammatory bowel disease mouse model was established using 4-week-old juvenile mice. Disease activity index and histopathological damage scores were determined using hematoxylin and eosin (H&E) staining. Tarm1, F4/80, CD68, and CD86 levels were detected using qPCR, western blotting, and immunofluorescence. Trans epithelial electric resistance (TEER) was detected using the transwell assay.
Results:
Results revealed that juvenile colitis mice fed 4% DSS drinking water had increased Tarm1 expression in the colon tissue, increased macrophage M1 polarization, higher expression of pro-inflammatory cytokines, and an impaired intestinal mucosal barrier, compared with the control group. Tarm1-knockdown RAW264.7 cells inhibited lipopolysaccharide (LPS)-induced M1 polarization and attenuated barrier damage in co-cultured intestinal epithelial cells.
Conclusion:
Tarm1 expression was increased in colonic tissues of juvenile mice with colitis, and LPS-induced M1 polarization and intestinal barrier damage were attenuated in Tarm1-knockdown RAW264.7 cells. This suggests that attenuation of Tarm1 expression is a potential target for pediatric inflammatory bowel disease therapy.
Insights
Tarm1 is elevated in juvenile mice with colitis, contributing to macrophage M1 polarization and intestinal barrier dysfunction. Reducing Tarm1 shows potential for treating pediatric inflammatory bowel disease.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Juvenile inflammatory bowel disease (IBD) presents unique challenges in understanding disease mechanisms.
- The role of Tarm1 in pediatric IBD and its impact on intestinal barrier integrity remains largely unexplored.
Purpose of the Study:
- To investigate the function of Tarm1 in a dextran sulfate sodium (DSS)-induced colitis model in juvenile mice.
- To elucidate the mechanisms by which Tarm1 influences intestinal barrier function during pediatric colitis.
Main Methods:
- Established a DSS-induced colitis model in 4-week-old juvenile mice.
- Assessed disease activity and histopathology via H&E staining.
- Quantified Tarm1, F4/80, CD68, and CD86 expression using qPCR, Western blotting, and immunofluorescence.
- Measured trans epithelial electric resistance (TEER) to evaluate intestinal barrier function.
Main Results:
- Juvenile mice with DSS-induced colitis exhibited increased colonic Tarm1 expression, elevated macrophage M1 polarization, and heightened pro-inflammatory cytokines.
- These mice also displayed significant impairment of the intestinal mucosal barrier.
- Tarm1 knockdown in RAW264.7 cells suppressed lipopolysaccharide (LPS)-induced M1 polarization and mitigated barrier damage in co-cultured intestinal cells.
Conclusions:
- Tarm1 expression is upregulated in the colonic tissues of juvenile mice suffering from colitis.
- Reducing Tarm1 expression in macrophages attenuated LPS-induced M1 polarization and intestinal barrier damage.
- Targeting Tarm1 presents a promising therapeutic strategy for pediatric inflammatory bowel disease.
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