Inflammation-associated pathways are active in intestinal epithelial cells (IECs) and contribute to the pathogenesis of colorectal cancer (CRC). Calcineurin, a phosphatase required for the activation of the nuclear factor of activated T cells (NFAT) family of transcription factors, shows increased expression in CRC. We therefore investigated the role of calcineurin in intestinal tumor development. We demonstrate that calcineurin and NFAT factors are constitutively expressed by primary IECs and selectively activated in intestinal tumors as a result of impaired stratification of the tumor-associated microbiota and toll-like receptor signaling. Epithelial calcineurin supports the survival and proliferation of cancer stem cells in an NFAT-dependent manner and promotes the development of intestinal tumors in mice. Moreover, somatic mutations that have been identified in human CRC are associated with constitutive activation of calcineurin, whereas nuclear translocation of NFAT is associated with increased death from CRC. These findings highlight an epithelial cell–intrinsic pathway that integrates signals derived from the commensal microbiota to promote intestinal tumor development.
As a potential measure to improve public health, this study aimed to reduce the sodium (Na) content of film-ripened, semihard Edam cheese to ≤0.4 g Na/100 g (≤1 g NaCl/100 g), while retaining typical quality and safety characteristics. For this, mineral salt substitutions containing potassium (K) were compared with simple NaCl reduction in brine, alongside an adjustment of starter cultures in an effort to enhance taste. Desired Na and K values were achieved, and microbial quality was not compromised in Na-reduced Edam after six weeks of ripening. However, all Na-reduced cheeses tasted bitter and were therefore organoleptically unsatisfactory.
Lactose solutions of up to 50% (w/v) were incubated with lactases and glucose isomerases for subsequent implementation in dairy product samples to enhance sweetness. A degree of hydrolysis of >90% and of isomerisation of 50% were attainable. The sensory sweetening power of lactose in solutions of up to 50% (w/v) can be enhanced 2–3 times. Based on sensory experiments, application of this bi‐enzymatic system in yoghurt and pudding samples allowed for a 10–20% (w/w) reduction in the total sugar content, whilst retaining equal sweetness. The growth of yoghurt starter cultures was not affected, yet furosine formation more than doubled in high heated, enzyme‐modified milk.
The reformulation of dairy products to contain less added sugar can contribute to reducing sugar consumption, thereby reducing the risk of non-communicable diseases. The objective of this study was to investigate the microbial ecology of reformulated yoghurt, which was produced using bi-enzymatic modification of lactose to increase its sweetness by a factor of 2–3. Ultimately, this reformulation strategy could reduce the amount of added sugar needed for equal sweetness of the end product. The bi-enzymatic modification relied on utilisation of a β-galactosidase enzyme to convert the milk sugar lactose to galactose and glucose, followed by the enzymatic conversion of the glucose moiety to fructose using a glucose isomerase. The microbial ecology of reformulated yoghurt produced with two mixed starter culture preparations containing either Streptococcus ( S .) thermophilus and Lactobacillus ( Lb .) delbrueckii or S. thermophilus , Lb. acidophilus and Bifidobacterium sp. strains, was analysed during fermentation and cool storage using 16S rRNA based metagenomics. None of the yoghurt samples showed a significant difference in microbial composition between sweetness-enhanced and regular milk at all sampling time points during manufacture and storage of yoghurt. However, a significant difference between the microbiota of inoculated milk before and after fermentation was observed. In both types of yoghurt, the starter culture genera dominated the microbial ecology at the end of fermentation as expected, reducing the possibility of growth of potentially pathogenic or spoilage bacteria possibly resulting from a changed carbohydrate spectrum.
Sodium intake is a major risk factor for non-communicable diseases. Consequently, reformulation of cheeses such as Edam to contain less sodium may contribute to lowering disease risk. However, sodium is essential for cheese manufacture, influencing starter culture bacteria activity and abundance during fermentation. This study aimed to assess the microbial diversity of reformulated Edam cheese samples with a reduced sodium content using culture-independent technique. The microbial diversity of samples produced using simple sodium reduction, as well as by substituting salt with a mineral salt compound containing potassium, were analysed in comparison to regular control Edam samples during manufacture and the subsequent 6-week ripening period using 16S rDNA metagenomics. In addition, a challenge test using Listeria (List.) innocua as a surrogate species for List. monocytogenes was performed. Reducing sodium content did not influence the microbiological composition of reformulated samples in comparison to that of regular samples. The starter culture bacteria dominated the microbial diversity and no increase in spoilage or potentially pathogenic bacterial growth was detected, including that of List. innocua. From a microbiological perspective, it can be concluded that lowering sodium content in Edam samples without affecting the microbial composition is achievable through simple sodium reduction and through implementation of a mineral salt replacement approach.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.