ArticleInflammatory bowel diseases2011
Small molecule tyrosine kinase inhibitors for the treatment of intestinal inflammation.
Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The central function and specific molecular mechanisms of the TLR4 pathway underlying impaired intestinal barrier in necrotizing enterocolitis.Biochemistry and biophysics reports · 2026Review
- FGF21 Depletion Attenuates Colitis through Intestinal Epithelial IL-22-STAT3 Activation in Mice.Nutrients · 2023Article
- Rab32-related antimicrobial pathway is involved in the progression of dextran sodium sulfate-induced colitis.FEBS open bio · 2018Article
- Tyrosine kinase inhibitors of Ripk2 attenuate bacterial cell wall-mediated lipolysis, inflammation and dysglycemia.Scientific reports · 2017Article
- Treatment of dextran sodium sulfate-induced experimental colitis by adoptive transfer of peritoneal cells.Scientific reports · 2015Article
- Atg16l1 is required for autophagy in intestinal epithelial cells and protection of mice from Salmonella infection.Gastroenterology · 2013Article
- Influence of Tyrphostin AG490 on the expression of diabetes-associated markers in human adipocytes.Immunogenetics · 2013Article
- p40phox expression regulates neutrophil recruitment and function during the resolution phase of intestinal inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Tyrphostin AG490 agent modestly but significantly prevents onset of type 1 in NOD mouse; implication of immunologic and metabolic effects of a Jak-Stat pathway inhibitor.Journal of clinical immunology · 2012Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe developed a series of dendritic cell autoimmune modulators (DCAMs) based on small molecule Flt3 receptor tyrosine kinase inhibitors (TKIs) for the inhibition of intestinal inflammation and oral delivery.
methodsDCAMs were administered orally during and after induction of dextran sodium sulfate (DSS)-induced colitis. Dendritic cell recruitment and inflammatory responses were determined in the mucosal immune system during acute intestinal inflammatory responses and mucosal recovery. Bone marrow-derived macrophages were utilized to define the mechanisms by which DCAMs can modify responses to microbial signals.
resultsOral doses of DCAMs prevented severe weight loss and mucosal inflammation associated with DSS colitis in mice. The presence of DCAMs increased the number of CD11c(+) PDCA1(+) dendritic cells, induced interleukin (IL)-10 expression, and reduced inflammatory cytokine expression in the mucosal immune system. Surprisingly, DCAMs regulated innate immune responses in macrophages resulting in the inhibition of tumor necrosis factor alpha (TNF-α) production and the induction of IL-10 expression during Toll-like receptor-mediated signaling.
conclusionsWe identified two new imidazoacridinone derivatives that protect mice from severe colitis and promote mucosal recovery by enhancing protective cytokine production while inhibiting proinflammatory stimuli during microbial recognition. These compounds are promising candidates for further development into potent orally available drugs for the prevention of colitis and promotion of mucosal recovery.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.