Effect of reduction of sodium content on the microbial ecology of Edam cheese samples.

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.

Microbial composition of sweetness-enhanced yoghurt during fermentation and storage.

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 ß-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.

Epithelial calcineurin controls microbiota-dependent intestinal tumor development.

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.