ArticleExperimental and therapeutic medicine2023
CD73 blockade alleviates intestinal inflammatory responses by regulating macrophage differentiation in ulcerative colitis.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Lung microbiota dysbiosis exacerbates influenza virus infection.Microbiome · 2026Article
- Impact of Zinc-Dependent Enzymes on Zinc Deficiency and Inflammatory Response in Ulcerative Colitis.Journal of gastroenterology and hepatology · 2026Observational
- CD73 Blockade Aggravate Dextran-Sodium-Sulfate-Induced Colitis via Down Regulating Inosine.Journal of inflammation research · 2026Article
- Purinergic signaling in the gut neuro-glial-immune axis: mechanisms of homeostasis, inflammation, and gastrointestinal dysfunction.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- N6-methyladenosine (m6A)-forming enzyme METTL3 controls UAF1 stability to promote inflammation in a model of colitis by stimulating NLRP3.Scientific reports · 2025Article
- Article
- Gene expression alterations of purinergic signaling components in obesity-associated intestinal low-grade inflammation in type 2 diabetes.Purinergic signalling · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ulcerative colitis (UC) is a type of inflammatory bowel disease characterized by excessive and persistent inflammation. Intestinal macrophages play a considerable role in regulating inflammatory immune reactions in the gut mucosa. It has previously been reported that CD73 is related to the pathogenesis of inflammatory or immune-related diseases; however, the roles of CD73 in UC remain unclear. In this study, CD73 expression in the inflamed mucosa of patients with UC was examined using reverse transcription-quantitative PCR (RT-qPCR), western blotting, and immunohistochemistry. Adenosine 5'-(α, β-methylene) diphosphate (APCP) was used to block the expression of CD73. Furthermore, the mRNA levels of proinflammatory mediators associated with macrophages following the blocking of CD73 were examined using RT-qPCR. Finally, the regulatory function of CD73 in intestinal inflammation was assessed by administering APCP in a mouse model of dextran sulfate sodium salt (DSS)-induced colitis. Notably, it was found that CD73 expression was significantly increased in the colonic mucosal tissues of patients with UC. Blockade of CD73 inhibited the expression of pro-inflammatory cytokines but promoted the production of anti-inflammatory cytokines in macrophages, while its promotion of M2 macrophage polarization was also verified.
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Registered trials
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