scholarly journals Impact of the Food Additive Titanium Dioxide (E171) on Gut Microbiota-Host Interaction

2019 ◽  
Vol 6 ◽  
Author(s):  
Gabriela Pinget ◽  
Jian Tan ◽  
Bartlomiej Janac ◽  
Nadeem O. Kaakoush ◽  
Alexandra Sophie Angelatos ◽  
...  
2019 ◽  
Vol 6 ◽  
Author(s):  
Gabriela Pinget ◽  
Jian Tan ◽  
Bartlomiej Janac ◽  
Nadeem O. Kaakoush ◽  
Alexandra Sophie Angelatos ◽  
...  

Author(s):  
Emanuele Rinninella ◽  
Marco Cintoni ◽  
Pauline Raoul ◽  
Vincenzina Mora ◽  
Antonio Gasbarrini ◽  
...  

Background: Titanium dioxide (TiO2) is used as a food additive in pastries, sweets, and sauces. It is recognized as safe by food safety authorities, but in recent years, governments and scientists have raised concerns about its genotoxicity. This systematic review aims to assess the potential associations between food TiO2 exposure and microbiota composition and functions. Methods: A systematic literature search was performed up to December 2020 in PubMed, Web of Science, and Scopus databases. The PRISMA guidelines followed. The risk of bias was assessed from ARRIVE and SYRCLE tools. Results: A total of 18 animal studies were included (n = 10 mice, n = 5 rats, n = 2 fruit flies, n = 1 silkworm). Studies varied significantly in protocols and outcomes assessment. TiO2 exposure might cause variations in abundance in specific bacterial species and lead to gut dysfunctions such as a reduction in SCFAs levels, goblet cells and crypts, mucus production, and increased biomarkers of intestinal inflammation. Conclusions: Although the extrapolation of these results from animals to humans remains difficult, this review highlights the key role of gut microbiota in gut nanotoxicology and stimulates discussions on the safe TiO2 use in food and dietary supplements. This systematic review was registered at PROSPERO as CRD42020223968.


2021 ◽  
Vol 22 (2) ◽  
pp. 772
Author(s):  
Javier Conde ◽  
Marlene Schwarzfischer ◽  
Egle Katkeviciute ◽  
Janine Häfliger ◽  
Anna Niechcial ◽  
...  

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO2) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO2 and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 (Ptpn2) and their role in the development of intestinal inflammation. Dextran sodium sulphate (DSS)-induced acute colitis was performed in mice lacking the expression of Ptpn2 in myeloid cells (Ptpn2LysMCre) or their wild type littermates (Ptpn2fl/fl) and exposed to the microparticle TiO2. The impact of Ptpn2 on TiO2 signalling pathways and TiO2-induced IL-1β and IL-10 levels were studied using bone marrow-derived macrophages (BMDMs). Ptpn2LysMCre exposed to TiO2 exhibited more severe intestinal inflammation than their wild type counterparts. This effect was likely due to the impact of TiO2 on the differentiation of intestinal macrophages, suppressing the number of anti-inflammatory macrophages in Ptpn2 deficient mice. Moreover, we also found that TiO2 was able to induce the secretion of IL-1β via mitogen-activated proteins kinases (MAPKs) and to repress the expression of IL-10 in bone marrow-derived macrophages via MAPK-independent pathways. This is the first evidence of the cooperation between the genetic risk factor Ptpn2 and the environmental factor TiO2 in the regulation of intestinal inflammation. The results presented here suggest that the ingestion of certain industrial compounds should be taken into account, especially in individuals with increased genetic risk


Author(s):  
Ewa Baranowska-Wójcik ◽  
Dominik Szwajgier ◽  
Klaudia Gustaw

AbstractFood-grade titanium dioxide (TiO2) containing a nanoparticle fraction (TiO2 NPs-nanoparticles) is widely used as a food additive (E171 in the EU). In recent years, questions concerning its effect on the gastrointestinal microbiota have been raised. In the present study, we examined interactions between bacteria and TiO2. The study involved six pathogenic/opportunistic bacterial strains and four different-sized TiO2 types: three types of food-grade E171 compounds and TiO2 NPs (21 nm). Each bacterial strain was exposed to four concentrations of TiO2 (60, 150, 300, and 600 mg/L TiO2). The differences in the growth of the analyzed strains, caused by the type and concentration of TiO2, were observed. The growth of a majority of the strains was shown to be inhibited after exposure to 300 and 600 mg/L of the food-grade E171 and TiO2 NPs.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yongliang Zhang ◽  
Shumin Duan ◽  
Ying Liu ◽  
Yun Wang

Abstract Objective Up to 44% of particulates of food-grade titanium dioxide (TiO2) are in nanoscale, while the effect and combined effect of which with other substances on intestinal barrier haven’t been fully understood yet. This study is aimed to study the effect of two kinds of TiO2 nanoparticles (TiO2 NPs and TiO2 MPs) on intestinal barrier functions, to reveal the combined effect of TiO2 NPs and Lipopolysaccharide (LPS) on intestinal barrier. Methods Male ICR mice were randomly divided into 18 groups (3 feed types * 3 exposure length * 2 LPS dosage) and were fed with normal or TiO2-mixed feed (containing 1% (mass fraction, w/w) TiO2 NPs or TiO2 MPs) for 1, 3, 6 months, followed by a single oral administration of 0 or 10 mg/(kg body weight) LPS. Four hours later, the transportation of TiO2, the intestinal barrier functions and the inflammatory response were evaluated. Results Both TiO2 notably increased the intestinal villi height / crypt depth ratios after 1 and 3 months of exposure, and increased the expression of ileal tight junction proteins (ZO-1 and occludin) after 1 month of exposure. After 6 months of exposure, TiO2 NPs led to reduced feed consumption, TiO2 MPs caused spare microvilli in small intestine and elevated Ti content in the blood cells. The intestinal permeability didn’t change in both TiO2 exposed groups. After LPS administration, we observed altered intestinal villi height / crypt depth ratios, lowered intestinal permeability (DAO) and upregulated expression of ileal ZO-1 in both (TiO2 +LPS) exposed groups. There are no significant changes of ileal or serum cytokines except for a higher serum TNF-α level in LPS treated group. The antagonistic effect was found between TiO2 NPs and LPS, but there are complicated interactions between TiO2 MPs and LPS. Conclusion Long-term intake of food additive TiO2 could alter the intestinal epithelial structure without influencing intestinal barrier function. Co-exposure of TiO2 and LPS would enhance intestinal barrier function without causing notable inflammatory responses, and there is antagonistic effect between TiO2 NPs and LPS. All the minor effects observed might associate with the gentle exposure method where TiO2 being ingested with feed.


2021 ◽  
Author(s):  
Matthew P. Ostrowski ◽  
Sabina Leanti La Rosa ◽  
Benoit J. Kunath ◽  
Andrew Robertson ◽  
Gabriel Pereira ◽  
...  

SummaryThe diets of industrialized countries reflect the increasing use of processed foods, often with the introduction of novel food additives. Xanthan gum is a complex polysaccharide with unique rheological properties that have established its use as a widespread stabilizer and thickening agent1. However, little is known about its direct interaction with the gut microbiota, which plays a central role in digestion of other, chemically-distinct dietary fiber polysaccharides. Here, we show that the ability to digest xanthan gum is surprisingly common in industrialized human gut microbiomes and appears to be contingent on the activity of a single bacterium that is a member of an uncultured bacterial genus in the family Ruminococcaceae. We used a combination of enrichment culture, multi-omics, and recombinant enzyme studies to identify and characterize a complete pathway in this uncultured bacterium for the degradation of xanthan gum. Our data reveal that this keystone degrader cleaves the xanthan gum backbone with a novel glycoside hydrolase family 5 (GH5) enzyme before processing the released oligosaccharides using additional enzymes. Surprisingly, some individuals harbor a Bacteroides species that is capable of consuming oligosaccharide products generated by the keystone Ruminococcaceae or a purified form of the GH5 enzyme. This Bacteroides symbiont is equipped with its own distinct enzymatic pathway to cross-feed on xanthan gum breakdown products, which still harbor the native linkage complexity in xanthan gum, but it cannot directly degrade the high molecular weight polymer. Thus, the introduction of a common food additive into the human diet in the past 50 years has promoted the establishment of a food chain involving at least two members of different phyla of gut bacteria.


2018 ◽  
Vol 12 ◽  
Author(s):  
James L Alexander ◽  
Alasdair J Scott ◽  
Anna L Pouncey ◽  
Julian Marchesi ◽  
James Kinross ◽  
...  

Author(s):  
Sophie Boutillier ◽  
Sophie Fourmentin ◽  
Blandine Laperche

2020 ◽  
Vol 8 (1) ◽  
pp. 111 ◽  
Author(s):  
Weida Wu ◽  
Li Zhang ◽  
Bing Xia ◽  
Shanlong Tang ◽  
Lei Liu ◽  
...  

Inulin (INU) is a non-digestible carbohydrate, known for its beneficial properties in metabolic disorders. However, whether and how gut microbiota in its regulation contributes to host metabolism has yet to be investigated. We conduct this study to examine the possible associations between the gut microbiota and circulating gut microbiota–host co-metabolites induced by inulin interventions. Plasma and intestinal site samples were collected from the pigs that have consumed inulin diet for 60 days. High-throughput sequencing was adopted for microbial composition, and the GC-TOF-MS-based metabolomics were used to characterize featured plasma metabolites upon inulin intervention. Integrated multi-omics analyses were carried out to establish microbiota–host interaction. Inulin consumption decreased the total cholesterol (p = 0.04) and glucose (p = 0.03) level in serum. Greater β-diversity was observed in the cecum and colon of inulin-fed versus that of control-fed pigs (p < 0.05). No differences were observed in the ileum. In the cecum, 18 genera were altered by inulin, followed by 17 in the colon and 6 in the ileum. Inulin increased propionate, and isobutyrate concentrations but decreased the ratio of acetate to propionate in the cecum, and increased total short fatty acids, valerate, and isobutyrate concentrations in the colon. Metabolomic analysis reveals that indole-3-propionic acid (IPA) was significantly higher, and the branched-chain amino acids (BCAA), L-valine, L-isoleucine, and L-leucine are significantly lower in the inulin groups. Mantel test and integrative analysis revealed associations between plasma metabolites (e.g., IPA, BCAA, L-tryptophan) and inulin-responsive cecal microbial genera. These results indicate that the inulin has regional effects on the intestine microbiome in pigs, with the most pronounced effects occurring in the cecum. Moreover, cecum microbiota plays a pivotal role in the modulation of circulating host metabolites upon inulin intervention


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