ArticleInternational journal of molecular medicine2018
Tumor necrosis factor-α acts reciprocally with solute carrier family 26, member 3, (downregulated-in-adenoma) and reduces its expression, leading to intestinal inflammation.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Congenital chloride diarrhea clinical features and management: a systematic review.Pediatric research · 2021Pooled it
- n-3 Polyunsaturated Fatty Acids Improve DSS-Induced Acute Colitis in Mice via Intestinal Barrier Fortification and Gut Microbiome Modulation.Digestive diseases and sciences · 2026Article
- Inhibition of adenylyl cyclase 1 or exchange protein activated by cAMP restores ATP-sensitive potassium channel activity after chronic opioid exposure.British journal of pharmacology · 2026Article
- Temporal transcriptomic profiling identifies core regulators in cytokine-induced gut barrier disruption in differentiated Caco-2 cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Case Report: Congenital chloride diarrhea in a prepubertal girl with perianal fistula and colonic ulcers.Frontiers in pediatrics · 2026Article
- Breaking Down Barriers: Epithelial Contributors to Monogenic IBD Pathogenesis.Inflammatory bowel diseases · 2024Review
- Bicarbonate secretion and acid/base sensing by the intestine.Pflugers Archiv : European journal of physiology · 2024Review
- Review
- Multiple Regulatory Signals and Components in the Modulation of Bicarbonate Transporters.Pharmaceutics · 2024Review
- GelNB molecular coating as a biophysical barrier to isolate intestinal irritating metabolites and regulate intestinal microbial homeostasis in the treatment of inflammatory bowel disease.Bioactive materials · 2023Article
- Diagnostic Challenge of Congenital Chloride Diarrhea and Ulcerative Colitis Overlap in an Adult Misdiagnosed with Bartter Syndrome: Case Report and Literature Review.The American journal of case reports · 2022Review
- Epithelial dysfunction is prevented by IL-22 treatment in a Citrobacter rodentium-induced colitis model that shares similarities with inflammatory bowel disease.Mucosal immunology · 2022Article
- Ulcerative Colitis: Novel Epithelial Insights Provided by Single Cell RNA Sequencing.Frontiers in medicine · 2022Review
- Pathophysiological role of ion channels and transporters in gastrointestinal mucosal diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Development of Crohn's Disease in a Child WithAnnals of laboratory medicine · 2021Article
- Congenital chloride-losing diarrhoea and Crohn's disease: a diagnostic and therapeutic challenge.Frontline gastroenterology · 2021Article
- Autotaxin stimulates LPA2 receptor in macrophages and exacerbates dextran sulfate sodium-induced acute colitis.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Therapeutic Mechanism of Macrophage Inflammatory Protein 1 α Neutralizing Antibody (CCL3) in Clostridium difficile Infection in Mice.The Journal of infectious diseases · 2020Article
- Adaptation to inflammatory acidity through neutrophil-derived adenosine regulation of SLC26A3.Mucosal immunology · 2020Article
- Gene Expression Profiling of Mediators Associated with the Inflammatory Pathways in the Intestinal Tissue from Patients with Ulcerative Colitis.Mediators of inflammation · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Solute carrier family 26, member 3 (Slc26a3), also termed downregulated-in-adenoma (DRA) is a member of the Slc26 family of anion transporters and is mutated in congenital chloride diarrhea. Our previous study demonstrated that DRA deficiency is associated with severely reduced colonic HCO3‑ secretion, a loss of colonic fluid absorption, a lack of a firmly adherent mucus layer and a severely reduced colonic mucosal resistance to dextran sodium sulfate (DSS) damage. However, the direct effect of mediators that trigger intestinal inflammatory factors on DRA has not been fully investigated. Tumor necrosis factor (TNF)‑α is a central mediator of intestinal inflammation in inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease. However, to the best of our knowledge, whether TNF‑α acts reciprocally with DRA leading to the development of gut inflammation in IBD has not been reported. The present study identified that the expression level of DRA was reduced in active UC patients and DSS‑induced colitis mice with high expression levels of TNF‑α identified in the peripheral blood serum. In addition, TNF‑α may affect the expression level of DRA in human colonic Caco2BBE cells in a dose‑dependent manner, including in DRA overexpressed Caco2BBE cells. Furthermore, knockdown of TNF‑α in Caco2BBE cells led to a higher expression level of DRA and a markedly reduced secretion of TNF‑α in the culture media. In addition, knockdown of DRA in Caco2BBE cells led to a higher secretion of TNF‑α in the culture media compared with the control cells, which could be reversed by overexpression of DRA. Overall, these results indicate that TNF‑α may act reciprocally with DRA, leading to the development of intestinal inflammation. Based on the pivotal position of TNF‑α in IBD, DRA is hypothesized to have therapeutic potential against colitis serving as an important target.
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