ArticleThe Journal of biological chemistry2010
Tumor necrosis factor alpha-induced inflammation is increased but apoptosis is inhibited by common food additive carrageenan.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 46 citations in OpenAlex.
- Development of Triamcinolone Acetonide-Loaded Nanoparticles for Inflammatory Knee Arthritis Treatment.International journal of nanomedicine · 2026Article
- Carrageenan and TLR4 Crosstalk: A Comprehensive Review of Inflammatory Responses in Animal Models.Recent advances in inflammation & allergy drug discovery · 2025Review
- Review
- Inherited Human BCL10 Deficiencies.Journal of clinical immunology · 2023Review
- Nanotechnology-driven improvisation of red algae-derived carrageenan for industrial and bio-medical applications.World journal of microbiology & biotechnology · 2023Review
- Personalized Dietary Regimens for Inflammatory Bowel Disease: Current Knowledge and Future Perspectives.Pharmacogenomics and personalized medicine · 2023Review
- Food Emulsifiers and Metabolic Syndrome: The Role of the Gut Microbiota.Foods (Basel, Switzerland) · 2022Review
- Mechanism of Glucose Water as a Neural Injection: A Perspective on Neuroinflammation.Life (Basel, Switzerland) · 2022Article
- Food and Food Groups in Inflammatory Bowel Disease (IBD): The Design of the Groningen Anti-Inflammatory Diet (GrAID).Nutrients · 2021Review
- Molecular Mapping of Hydrogen Sulfide Targets in Normal Human Keratinocytes.International journal of molecular sciences · 2020Article
- Lipoprotein Lipase Inhibitor, Nordihydroguaiaretic Acid, Aggravates Metabolic Phenotypes and Alters HDL Particle Size in the Western Diet-Fed db/db Mice.International journal of molecular sciences · 2019Article
- Distinct Effects of Carrageenan and High-Fat Consumption on the Mechanisms of Insulin Resistance in Nonobese and Obese Models of Type 2 Diabetes.Journal of diabetes research · 2019Article
- The Role of Carrageenan and Carboxymethylcellulose in the Development of Intestinal Inflammation.Frontiers in pediatrics · 2017Review
- Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity.The Journal of allergy and clinical immunology · 2015Review
- Death-associated protein kinase controls STAT3 activity in intestinal epithelial cells.The American journal of pathology · 2013Article
- Intestinal protein expression profile identifies inflammatory bowel disease and predicts relapse.International journal of clinical and experimental pathology · 2013Article
- Carrageenan-induced transient inflammation in a rabbit knee model: molecular changes consistent with an early osteoarthritis phenotype.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor (TNF)-α, a homotrimeric, pleiotropic cytokine, is secreted in response to inflammatory stimuli in diseases such as rheumatoid arthritis and inflammatory bowel disease. TNF-α mediates both apoptosis and inflammation, stimulating an inflammatory cascade through the non-canonical pathway of NF-κB activation, leading to increased nuclear RelB and p52. In contrast, the common food additive carrageenan (CGN) stimulates inflammation through both the canonical and non-canonical pathways of NF-κB activation and utilizes the adaptor molecule BCL10 (B-cell leukemia/lymphoma 10). In a series of experiments, colonic epithelial cells and mouse embryonic fibroblasts were treated with TNF-α and carrageenan in order to simulate the possible effects of exposure to dietary CGN in the setting of a TNF-α-mediated inflammatory disease process. A marked increase in secretion of IL-8 occurred, attributable to synergistic effects on phosphorylated NF-κB-inducing kinase (NIK) in the non-canonical pathway. TNF-α induced the ubiquitination of TRAF2 (TNF receptor-associated factor 2), which interacts with NIK, and CGN induced phosphorylation of BCL10, leading to increased NIK phosphorylation. These results suggest that TNF-α and CGN in combination act to increase NIK phosphorylation, thereby increasing activation of the non-canonical pathway of NF-κB activation. In contrast, the apoptotic effects of TNF-α, including activation of caspase-8 and PARP-1 (poly(ADP-ribose) polymerase 1) fragmentation, were markedly reduced in the presence of CGN, and CGN caused reduced expression of Fas. These findings demonstrate that exposure to CGN drives TNF-α-stimulated cells toward inflammation rather than toward apoptotic cell death and suggest that CGN exposure may compromise the effectiveness of anti-TNF-α therapy.
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Registered trials
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.