ArticleWorld journal of gastroenterology2018
Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice.
Article in World journal of gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Mesenchymal stem cells against intestinal ischemia-reperfusion injury: a systematic review and meta-analysis of preclinical studies.Stem cell research & therapy · 2022Pooled it
- High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications.Chinese medical journal · 2026Review
- SGK1 signaling: an important modulator of CFTR function and early immune response in mouse intestine.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Role of Serum/Glucocorticoid-Regulated Kinase 1 (SGK1) in Immune and Inflammatory Diseases.Inflammation · 2023Review
- Schisandrin protects against ulcerative colitis by inhibiting the SGK1/NLRP3 signaling pathway and reshaping gut microbiota in mice.Chinese medicine · 2023Article
- Cell-penetrating TLR inhibitor peptide alleviates ulcerative colitis by the functional modulation of macrophages.Frontiers in immunology · 2023Article
- The modulatory effect of high salt on immune cells and related diseases.Cell proliferation · 2022Review
- Neuroprotective Role of Lactoferrin during Early Brain Development and Injury through Lifespan.Nutrients · 2022Review
- Jianpi Qinghua Fomula alleviates insulin resistance via restraining of MAPK pathway to suppress inflammation of the small intestine in DIO mice.BMC complementary medicine and therapies · 2022Article
- Metabolic Shifts as the Hallmark of Most Common Diseases: The Quest for the Underlying Unity.International journal of molecular sciences · 2021Article
- On the Role of Salt in Immunoregulation and Autoimmunity.Mediterranean journal of rheumatology · 2021Article
- Common contributing factors to COVID-19 and inflammatory bowel disease.Toxicology reports · 2021Article
- Inhibitor of Differentiation-2 Protein Ameliorates DSS-Induced Ulcerative Colitis by Inhibiting NF-κB Activation in Neutrophils.Frontiers in immunology · 2021Article
- Inactivation of paracellular cation-selective claudin-2 channels attenuates immune-mediated experimental colitis in mice.The Journal of clinical investigation · 2020Article
- Metabolic and immunologic control of intestinal cell function by mTOR.International immunology · 2020Review
- From Maternal Diet to Neurodevelopmental Disorders: A Story of Neuroinflammation.Frontiers in cellular neuroscience · 2020Review
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the influence of high salt on dextran sulfate sodium (DSS)-induced colitis in mice and explore the underlying mechanisms of this effect.
methodsDSS and NaCl were used to establish the proinflammatory animal model. We evaluated the colitis severity. Flow cytometry was employed for detecting the frequencies of Th1, macrophages and Tregs in spleen, mesenteric lymph node and lamina propria. The important role of macrophages in the promotion of DSS-induced colitis by NaCl was evaluated by depleting macrophages with clodronate liposomes. Activated peritoneal macrophages and lamina propria mononuclear cells (LPMCs) were stimulated with NaCl, and proteins were detected by western blotting. Cytokines and inflammation genes were analyzed by enzyme-linked immunosorbent assay and RT-PCR, respectively.
resultsThe study findings indicate that NaCl up-regulates the frequencies of CD11b
conclusionProinflammatory macrophages may play an essential role in the onset and development of NaCl-promoted inflammation in DSS-induced colitis. The underlining mechanism involves up-regulation of the p38/MAPK axis.
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Registered trials
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