scholarly journals Effect of TiO2 on Selected Pathogenic and Opportunistic Intestinal Bacteria

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.

Author(s):  
Chunyang Li ◽  
Chuanxin Ma ◽  
Heping Shang ◽  
Jason C. White ◽  
David Julian McClements ◽  
...  

E171 reduced Fe bioaccessibility of spinach in a simulated gastrointestinal tract via two mechanisms: the inhibition of α-amylase activity and adsorption of released Fe from spinach.


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


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.


1969 ◽  
Vol 172 (1029) ◽  
pp. 417-437 ◽  

Soon after the isolation of nodule bacteria in 1888, differences were recognized in the ability of bacterial strains to form nodules on particular host plants and in the nitrogen-fixing ability of the nodules so formed. These and other symbiotic heterogeneities were attributed, sometimes correctly, to bacterial strain differences, not then thought to be open to formal genetic analysis. The realization that the host plant was an essential component of this variability came only gradually, stimulated by observations of host varietal differences and by the demand for reliable and homogeneous material for experimental work. Only within the last two decades has host variability been studied by plant breeding, and bacterial strain differences by some of the methods of microbial genetics. This review, except for a brief reference to earlier work of some historic interest, will consider only genetic problems open to investigation by these methods. The developmental sequence in all legume nodules is broadly similar. The initial infection phases are followed by the induction of the nodule, the invasion of part of the nodular tissue and culminate in bacteroid formation and nitrogen fixation; the genetics of symbiosis will be considered in this context.


2013 ◽  
Vol 23 ◽  
pp. 83-90
Author(s):  
Seung Han Oh ◽  
In Young Na ◽  
Kyoung Hee Choi

Although titanium dioxide (TiO2) is an implantable biomaterial with its antibacterial activity, infection on TiO2 surfaces remains a problem for medical settings. According to our previous studies, curcumin, the main component of turmeric (Curcuma longa), partially hindered the attachment of Streptococcus mutans to human tooth surfaces. Therefore, it was examined whether several implant device-associated bacteria were able to adhere to nanosized TiO2 surfaces. In addition, the effect of curcumin on the bacterial adhesion was investigated. Bacterial strains were cultured on pure Ti and TiO2 surfaces with various nanotube sizes in the absence or presence of curcumin and observed by scanning electron microscopy. Consequently, most bacteria adhered to Ti and TiO2 surfaces. However, curcumin increased the adhesion of bacteria including S. mutans. The results suggest that bacterial adhesion to implant titanium surfaces can be augmented via curcumin ingestion.


Author(s):  
Yu. O. Shulpekova ◽  
G. H. Babaeva ◽  
V. Yu. Rusyaev

Aim. This review aims to describe the nature of changes in the intestinal microbiota in irritable bowel syndrome (IBS) and provide a pathogenetic justification of the feasibility of a therapeutic impact on microbiota. General findings. An important aspect of the interaction of intestinal bacteria with the “host” cells is their contact with pattern recognition receptors of enterocytes, dendritic cell receptors, as well as a transcellular transport of antigens in the region of Peyer’s patches. The area of interaction of intestinal bacteria and the human body is not limited to the intestines. Intestinal bacteria demonstrate a significant humoral effect due to signalling molecules, some of which exhibit neurotransmitter properties. The study of the bacterial cross-feeding for various species, i.e. mutual use of nutrient substrates produced by bacteria of various species, is of a great interest. The development of a lowactivity inflammation in IBS can partly be explained by the increased interaction of flagellin with the corresponding receptor, as well as the influx of excess bacteria from the small intestine. The majority of studies on IBS have demonstrated the predominance of intestinal bacteria with pro-inflammatory potential (Enterobacteriaceae) and the lack of bacteria with a pronounced anti-inflammatory, antimicrobial and enzymatic action (Lactobacillus and Bifidobacterium), as well as increased mucus degradation. Similar changes are observed in inflammatory bowel diseases. Reduced microbial diversity increases susceptibility to intestinal infections and parasitoses, including those caused by protozoa conditionally pathogenic for adults, such as Blastocystis hominis hominis, Dientamoeba fragilis, Giardia lamblia. With the help of nutrition correction, the use of probiotics and functional foods containing certain probiotic strains, plant fibres (primarily psyllium) and, in some cases, nonabsorbable antibiotics, a positive effect can be achieved in a significant number of IBS patients. Recent works have shown that clinical improvement is accompanied by a change in the composition of the intestinal microbiota.Conclusion. For the pathogenetic treatment of irritable bowel syndrome, the use of non-drug treatment is justified, such as diet optimization and prescription of plant fibres and probiotic bacterial strains. The positive effect of such an approach is largely determined by modification of the intestinal microbiota composition. This opens up prospects for a further, more targeted impact on the intestinal microbiome.


2018 ◽  
Vol 120 ◽  
pp. 321-327 ◽  
Author(s):  
Ditte Marie Jensen ◽  
Gry Freja Skovsted ◽  
Jens Lykkesfeldt ◽  
Rasmus Dreier ◽  
Jais Oliver Berg ◽  
...  

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

Author(s):  
Naif Abdullah Al-Dhabi ◽  
Galal Ali Esmail ◽  
Abdul-Kareem Mohammed Ghilan ◽  
Mariadhas Valan Arasu

In this study, 23 bacterial strains were isolated from a Cadmium (Cd) contaminated soil in the industrial city, Riyadh of Saudi Arabia. Among these isolates six strains were found to withstand cadmium contamination and grow well. From the six isolates Pseudomonas sp. strain Al-Dhabi-122–127 were found to resist cadmium toxicity to a higher level. The isolates were subjected to biochemical and 16S rDNA gene sequence characterization to confirm their identification. The bacterial strain Al-Dhabi-124 showed 1.5 times higher Cd-degrading activity than Al-Dhabi-122 and Al-Dhabi-123, and Al-Dhabi-126 exhibited 3.5 times higher Cd-degrading activity, higher than the other strains. An atomic absorption spectrophotometer study showed that the strain Al-Dhabi-126 absorbed Cd, and that the bacterial strain Al-Dhabi-126 was found to tolerate cadmium level up to 2100 µg/mL. The bacterial strain Al-Dhabi-126 showed a maximum Cd removal efficacy at pH between 6.0 and 8.0. The efficacy decreased sharply after an increase in pH (9.0). An optimum temperature of 50 °C and pH 6.0 were found to be effective for the Cd removal process by the isolate. The study indicated that the bacterial strain Al-Dhabi-126 can be used effectively for the bioremediation of heavy metals like cadmium, a major toxic pollutant in industrial effluents.


2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S092-S092
Author(s):  
J Conde ◽  
M Schwarzfischer ◽  
E Katkeviciute ◽  
J Häfliger ◽  
A Niechcial ◽  
...  

Abstract Background Inflammatory bowel disease (IBD) is caused by a complex interaction among genetic, immunological, bacterial and environmental factors. In this scenario, protein tyrosine phosphatase non-receptor type-2 (PTPN2) has been recognised as a risk factor for the development of IBD and functional studies revealed a major role for this protein in the development of experimental colitis through the regulation of the inflammasome, among other processes. In the same way, a potential relationship between diet components and IBD was suggested. In fact, it was reported that the food additive titanium dioxide (TiO2) was able to induce inflammasome activation in vitro and increase colitis severity in vivo. These observations led us to hypothesise a putative relationship between PTPN2 and TiO2 that could explain the effects of this microparticle in the pathogenesis of bowel inflammation. Methods DSS colitis model was performed in mice lacking PTPN2 in myeloid cells and their wild-type littermates, treated or not with titanium dioxide. After that, histology studies, flow cytometry, expression analysis, ELISA and barrier function experiments were performed. Also, bone marrow-derived macrophages (BMDMs) were used for in vitro studies. Results Titanium dioxide was able to exacerbate DSS-induced colitis, especially in mice lacking PTPN2 in myeloid cells. Flow cytometry analysis of the lamina propria revealed significant changes in different immune cell populations such as macrophages. In vitro experiments using BMDMs revealed that TiO2 induced the activation of the inflammasome. Also, this microparticle down-regulated the expression of the anti-inflammatory cytokine IL-10 and these effects were mainly mediated by JNK and ERK kinases. Conclusions The food additive titanium dioxide seems to play a negative role in colitis development by affecting the production of pro- and anti-inflammatory mediators in macrophages. This study reveals a new mechanism by which a certain component of the diet modulates intestinal inflammation.


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