ArticleIn vitro cellular & developmental biology. Animal1998
Factors affecting Caco-2 intestinal epithelial cell interleukin-6 secretion.
Article in In vitro cellular & developmental biology. Animal, 1998. 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, 47 citations in OpenAlex.
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- Pro-Inflammatory Cytokines Trigger the Overexpression of Tumour-Related Splice Variant RAC1B in Polarized Colorectal Cells.Cancers · 2022Article
- The JAK Inhibitor Tofacitinib Rescues Intestinal Barrier Defects Caused by Disrupted Epithelial-macrophage Interactions.Journal of Crohn's & colitis · 2021Article
- Direct On-Chip Differentiation of Intestinal Tubules from Induced Pluripotent Stem Cells.International journal of molecular sciences · 2020Article
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- Thirty-eight-negative kinase 1 mediates trauma-induced intestinal injury and multi-organ failure.The Journal of clinical investigation · 2018Article
- Histone deacetylase-mediated regulation of the antimicrobial peptide hBD2 differs in intestinal cell lines and cultured tissue.Scientific reports · 2018Article
- IL-22 Enhances TNF-α- and IL-1-Induced CXCL8 Responses by Intestinal Epithelial Cell Lines.Inflammation · 2017Article
- ROCK activity affects IL-1-induced signaling possibly through MKK4 and p38 MAPK in Caco-2 cells.In vitro cellular & developmental biology. Animal · 2016Article
- CFTR Knockdown induces proinflammatory changes in intestinal epithelial cells.Journal of inflammation (London, England) · 2015Article
- The Value of Desmethylclozapine and Serum CRP in Clozapine Toxicity: A Case Report.Case reports in psychiatry · 2012Article
- Hepatocyte growth factor and keratinocyte growth factor enhance IL-1-induced IL-8 secretion through different mechanisms in Caco-2 epithelial cells.In vitro cellular & developmental biology. Animal · 2011Article
- Article
- Epithelial cells respond to proteolytic and non-proteolytic detachment by enhancing interleukin-6 responses.Immunology · 2002Article
- Small bowel review: normal physiology part 2.Digestive diseases and sciences · 2001Review
- Hepatocyte growth factor enhances IL-1beta stimulated IL-8 secretion by Caco-2 epithelial cells.In vitro cellular & developmental biology. AnimalArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Intestinal epithelial cells (IEC) have previously been shown to produce several cytokines including interleukin-6 (IL-6). However, many factors which may regulate IL-6 secretion by human IEC still remain a mystery due in part to the lack of appropriate model cell lines and the difficulty of culturing human IEC over long periods of time. We have determined that the human colonic carcinoma cell line Caco-2 is capable of secreting IL-6 when stimulated by the inflammatory cytokines IL-1beta or tumor necrosis factor-alpha (TNF-alpha), and stimulation of these cells with IL-1beta plus TNF-alpha induced a synergistic enhancement of IL-6 secretion. The inflammatory cytokine-induced enhancement in IL-6 secretion was greatest when the cells were cultured in a 10% CO2 atmosphere as compared to cells grown in 5% CO2, suggesting that environmental CO2 levels may affect IEC cytokine secretion. Finally, long-term culture of the Caco-2 cells to induce cellular differentiation had no effect on the capacity of these cells to produce IL-6, indicating that the regulation of IL-6 secretion was not affected by differentiation. Taken together, these studies provide important information on the factors which regulate IL-6 secretion by human IEC as they may contribute to the cytokine network during a mucosal inflammation. The results also suggest that the Caco-2 cell line is an appropriate model for further studies on the regulation of cytokine secretion by human IEC.
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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.