Titanium dioxide nanoparticles exacerbate DSS-induced colitis: role of the NLRP3 inflammasome
Pedro A. Ruiz,Belén Morón,Helen M. Becker,Silvia Lang,Kirstin Atrott,Marianne R. Spalinger,Michael Scharl,Kacper A. Wojtal,Anne Fischbeck-Terhalle,Isabelle Frey-Wagner,Martin Hausmann,Thomas Kraemer,Gerhard Rogler +12 more
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TLDR
Findings indicate that individuals with a defective intestinal barrier function and pre-existing inflammatory condition, such as IBD, might be negatively impacted by the use of TiO2 nanoparticles.Abstract:
Objective Western lifestyle and diet are major environmental factors playing a role in the development of IBD. Titanium dioxide (TiO 2 ) nanoparticles are widely used as food additives or in pharmaceutical formulations and are consumed by millions of people on a daily basis. We investigated the effects of TiO 2 in the development of colitis and the role of the nucleotide-binding oligomerisation domain receptor, pyrin domain containing (NLRP)3 inflammasome. Design Wild-type and NLRP3-deficient mice with dextran sodium sulfate-induced colitis were orally administered with TiO 2 nanoparticles. The proinflammatory effects of TiO 2 particles in cultured human intestinal epithelial cells (IECs) and macrophages were also studied, as well as the ability of TiO 2 crystals to traverse IEC monolayers and accumulate in the blood of patients with IBD using inductively coupled plasma mass spectrometry. Results Oral administration of TiO 2 nanoparticles worsened acute colitis through a mechanism involving the NLRP3 inflammasome. Importantly, crystals were found to accumulate in spleen of TiO 2 -administered mice. In vitro, TiO 2 particles were taken up by IECs and macrophages and triggered NLRP3-ASC-caspase-1 assembly, caspase-1 cleavage and the release of NLRP3-associated interleukin (IL)-1β and IL-18. TiO 2 also induced reactive oxygen species generation and increased epithelial permeability in IEC monolayers. Increased levels of titanium were found in blood of patients with UC having active disease. Conclusion These findings indicate that individuals with a defective intestinal barrier function and pre-existing inflammatory condition, such as IBD, might be negatively impacted by the use of TiO 2 nanoparticles.read more
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Food-grade TiO 2 impairs intestinal and systemic immune homeostasis, initiates preneoplastic lesions and promotes aberrant crypt development in the rat colon.
Sarah Bettini,Elisa Boutet-Robinet,Christel Cartier,Christine Coméra,Eric Gaultier,J. Dupuy,Nathalie Naud,Sylviane Taché,Patrick Grysan,Solenn Reguer,Nathalie Thieriet,Matthieu Réfrégiers,Dominique Thiaudière,Jean Pierre Cravedi,Marie Carrière,Jean-Nicolas Audinot,Fabrice Pierre,Laurence Guzylack-Piriou,Eric Houdeau +18 more
TL;DR: In rats orally exposed for one week to E171 at human relevant levels, titanium was detected in the immune cells of Peyer’s patches (PP) as observed with the TiO2-NP model NM-105, and these data should be considered for risk assessments of the susceptibility to Th17-driven autoimmune diseases and to colorectal cancer in humans exposed toTiO2 from dietary sources.
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Evolving role of diet in the pathogenesis and treatment of inflammatory bowel diseases
TL;DR: Progress in the field of microbiome and IBD has demonstrated that microbiome appears to play an important role in pathogenesis, and that diet may in turn impact the composition and functionality of the microbiome.
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Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation.
Jesus Cosin-Roger,Simona Simmen,Hassan Melhem,Kirstin Atrott,Isabelle Frey-Wagner,Martin Hausmann,Cheryl de Valliere,Marianne R. Spalinger,Patrick Spielmann,Roland H. Wenger,Jonas Zeitz,Stephan R. Vavricka,Gerhard Rogler,Pedro A. Ruiz +13 more
TL;DR: Hypoxia is shown to ameliorate intestinal inflammation in Crohn’s patients and murine colitis models by inhibiting mTOR/NLRP3 pathway and promoting autophagy, and it is suggested that hypoxia counteracts inflammation through the downregulation of the binding of mTOR and NLRP3 and activation of Autophagy.
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Redox signaling in the gastrointestinal tract.
TL;DR: Redox signaling plays a critical role in the physiology and pathophysiology of gastrointestinal tract and in colorectal cancer, and exhibits two Janus faces: on the one hand, NOX1 up-regulation and derived hydrogen peroxide enhance Wnt/β-catenin and Notch proliferating pathways; on the other hand, ROS may disrupt tumor progression through different pro-apoptotic mechanisms.
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Urbanization and the gut microbiota in health and inflammatory bowel disease.
TL;DR: The disparate patterns of the gut microbiota composition in rural and urban areas offer an opportunity to understand the contribution of a ‘rural microbiome’ in potentially protecting against the development of IBD.
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Food-grade TiO 2 impairs intestinal and systemic immune homeostasis, initiates preneoplastic lesions and promotes aberrant crypt development in the rat colon.
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