ArticleJournal of clinical laboratory analysis2022
Histone deacetylase 1 and 3 inhibitors alleviate colon inflammation by inhibiting Th17 cell differentiation.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Unraveling the drug resistance web in IBD: The gut microbiota-immunity-epigenetics axis.Gut microbes · 2026Review
- Pleiotropic Mucosal Innate Immune Memory in the Gastrointestinal Tract.International journal of molecular sciences · 2025Review
- Histone deacetylase in inflammatory bowel disease: novel insights.Therapeutic advances in gastroenterology · 2025Review
- Cross-talk between macrophages and gut microbiota in inflammatory bowel disease: a dynamic interplay influencing pathogenesis and therapy.Frontiers in medicine · 2024Review
- Genetic association and causal effects between inflammatory bowel disease and conjunctivitis.Frontiers in immunology · 2024Article
- Histone deacetylase 1 and 3 inhibitors alleviate colon inflammation by inhibiting Th17 cell differentiation.Journal of clinical laboratory analysis · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe etiology of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is not completely clear, but its pathogenesis is closely related to T helper 17 (Th17) cells. Several histone deacetylase (HDAC) inhibitors have been shown to exert potent anti-inflammatory effects and modulate Th17 cell polarization. Owing to the large variety and broad expression of HDACs, finding specific therapeutic targets for IBD is of clinical importance.
methodsThe proportions of Th17 cells and interleukin (IL)-17A produced between patients with UC and healthy volunteers were compared. The differentiation of human peripheral blood mononuclear cells (PBMCs) into Th17 cells was induced in vitro. Differentiated Th17 cells were treated with RGFP109 (RG), a selective inhibitor of HDAC1 and 3, to observe its effects on these cells. Subsequently, colitis was induced in mice and treated with RG. The proportion of Th17 cells, the severity of colitis in mice, and colon histopathology and immunohistochemistry were evaluated respectively.
resultsThe proportion of Th17 cells and IL-17A production was significantly increased in patients with UC than in healthy individuals. RG inhibited the differentiation of human PBMCs into Th17 cells and reduced IL-17A secretion in vitro. RG-treated colitis mice had a lower Th17 ratio, mild colon inflammation, and decreased expression of HDAC1 and 3 in the colon.
conclusionsHDAC1 and 3 inhibitors can modulate the differentiation of inflammatory Th17 cells, downregulate IL-17A levels, and exert anti-inflammatory effects in experimental colitis mice, indicating that HDAC1 and 3 may be potential therapeutic targets for patients with IBD.
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