ArticleDigestive diseases and sciences2007
The ICE inhibitor pralnacasan prevents DSS-induced colitis in C57BL/6 mice and suppresses IP-10 mRNA but not TNF-alpha mRNA expression.
Article in Digestive diseases and sciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 74 citations in OpenAlex.
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- Inflammatory Bowel Disease Increases the Severity of Myocardial Infarction after Acute Ischemia-Reperfusion Injury in Mice.Biomedicines · 2023Article
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- Pyroptosis-Induced Inflammation and Tissue Damage.Journal of molecular biology · 2022Review
- Compound loss of GSDMD and GSDME function is necessary to achieve maximal therapeutic effect in colitis.Journal of translational autoimmunity · 2022Article
- Inflammasomes and Colorectal Cancer.Cells · 2021Review
- Contradictory Effects of NLRP3 Inflammasome Regulatory Mechanisms in Colitis.International journal of molecular sciences · 2020Review
- Inflammasome inhibitors: promising therapeutic approaches against cancer.Journal of hematology & oncology · 2019Review
- NLRP3 inflammasome in colitis and colitis-associated colorectal cancer.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- MCC950, a specific small molecule inhibitor of NLRP3 inflammasome attenuates colonic inflammation in spontaneous colitis mice.Scientific reports · 2018Article
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- Free immunoglobulin light chain (FLC) promotes murine colitis and colitis-associated colon carcinogenesis by activating the inflammasome.Scientific reports · 2017Article
- Inflammasomes and intestinal inflammation.Mucosal immunology · 2017Review
- The AIM2 inflammasome is a central regulator of intestinal homeostasis through the IL-18/IL-22/STAT3 pathway.Cellular & molecular immunology · 2017Article
- Deoxycholic Acid Triggers NLRP3 Inflammasome Activation and Aggravates DSS-Induced Colitis in Mice.Frontiers in immunology · 2016Article
- IL-1 in Colon Inflammation, Colon Carcinogenesis and Invasiveness of Colon Cancer.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2015Article
- Protective role for caspase-11 during acute experimental murine colitis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Inflammasomes and intestinal homeostasis: regulating and connecting infection, inflammation and the microbiota.International immunology · 2014Review
- Nlrp3 activation in the intestinal epithelium protects against a mucosal pathogen.Mucosal immunology · 2014Article
- Small molecule-driven mitophagy-mediated NLRP3 inflammasome inhibition is responsible for the prevention of colitis-associated cancer.Autophagy · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously we demonstrated an ameliorating effect of the interleukin-1beta converting enzyme (ICE) inhibitor pralnacasan on dextran sulfate sodium (DSS)-induced colitis. This study investigates the effects of pralnacasan on cytokine expression in DSS-induced colitis. Colitis was induced by oral administration of DSS. Mice were treated intraperitoneally with the ICE inhibitor pralnacasan (50 mg/kg body weight twice daily). Body weight as well as the presence of occult blood or diarrhea was monitored daily. Subgroups were sacrificed at days 4, 8, and 11 after the beginning of DSS application. Cytokine profiles in colonic tissue were analyzed on the protein level by ELISA and on the mRNA level by real time RT-PCR. Administration of DSS led to an increase in IL-18, IL-12, TNF-alpha, and IFN-gamma protein as well as IP-10 and TNF-alpha mRNA. The increase in IL-18 and IFN-gamma was reduced by ICE inhibition. Pralnacasan prevented DSS-induced colitis in C57BL/6 mice. In C57BL/6 mice, the DSS-induced increase in IP-10 mRNA, but not TNF-alpha mRNA, was completely prevented by ICE inhibition. In conclusion, prevention of colitis in C57BL/6 mice was associated with a suppresion of IP-10 mRNA, but not TNF-alpha mRNA expression, indicating that IL-18-mediated cytokine production is a key element in the pathogenesis of DSS-induced colitis.
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