Fermentation represents a pivotal bioconversion process that enhances foodstuffs’ nutritional and sensory attributes while playing a crucial role in global food systems. Nevertheless, concerns about safety issues associated with microbial contamination and the production of biogenic amines are often understated. This review appraised recent advancements in fermentation technology, emphasising their association with the health and safety of fermented foods. Key advances include predictive microbiology models, in some cases achieving up to 95% accuracy in predicting microbial behaviour, and high-throughput sequencing (HTS) for microbial enrichment. In addition, advanced detection methods such as biosensors and PCR-based assays enable the rapid identification of contaminants, improving manufacturing processes and preserving product integrity. Advanced bioreactor technologies equipped with real-time monitoring systems have been shown to increase fermentation efficiency. Moreover, innovative packaging, artificial intelligence, machine learning models, and sensor technologies have optimised fermentation processes and contributed to tracking quality and safety in the blockchain technology supply chain, potentially reducing spoilage rates and showing a decrease in production times. This study also addresses regulatory frameworks essential for establishing robust safety protocols. Integrating advanced fermentation technologies is imperative to meet the growing global demand for safe fermented foods. Continuous research and innovation are needed to address safety challenges and promote industry practices prioritising health and quality, ensuring public safety and building consumer confidence in fermented products.

Background: Oat beta-glucans are polysaccharides, belonging to soluble fiber fraction, that show a wide spectrum of biological activity. The aim of this study was to evaluate the time-dependent antioxidative effect of chemically pure oat beta-glucan fractions, characterized by different molar mass, which were fed to animals with early stage of 2,4,6-trinitrobenzene sulfonic acid (TNBS) - induced colitis. Methods: The study was conducted on 150 adult male Sprague Dawley rats assigned to two groups—healthy control (H) and colitis (C) with colon inflammation induced by per rectum administration of TNBS. The animals from both groups were divided into 3 nutritional subgroups, receiving for 3, 7 or 21 days AIN-93M feed without beta-glucan (βG−) or with 1% (w/w) low molar mass oat beta-glucan (βGl+) or 1% (w/w) high molar mass oat beta-glucan (βGh+). After 3, 7 and 21 days, the animals were euthanized, peripheral blood was collected from the heart for further analysis. Results: The results of analyses performed on blood samples showed small changes in lymphocytes count and red blood cell parameters such as the number of red blood cell, mean corpuscular hemoglobin concentration and mean corpuscular volume (RBC, MCHC, MCV respectively) as well as normalization of antioxidant potential accompanying moderate inflammatory state of colon mucosa and submucosa. Conclusion: Oat beta-glucans exert an indirect antioxidant effect in animals with TNBS-induced colitis, with greater effectiveness in removing systemic effects of colon inflammation found for low molar mass oat beta-glucan.

Background: Crohn’s disease (CD) is characterized by chronic inflammation of the gastrointestinal tract with alternating periods of exacerbation and remission. The aim of this study was to determine the time-dependent effects of dietary oat beta-glucans on colon apoptosis and autophagy in the CD rat model. Methods: A total of 150 Sprague–Dawley rats were divided into two main groups: healthy control (H) and a TNBS (2,4,6-trinitrobenzosulfonic acid)-induced colitis (C) group, both including subgroups fed with feed without beta-glucans (βG−) or feed supplemented with low- (βGl) or high-molar-mass oat beta-glucans (βGh) for 3, 7, or 21 days. The expression of autophagy (LC3B) and apoptosis (Caspase-3) markers, as well as Toll-like (TLRs) and Dectin-1 receptors, in the colon epithelial cells, was determined using immunohistochemistry and Western blot. Results: The results showed that in rats with colitis, after 3 days of induction of inflammation, the expression of Caspase-3 and LC3B in intestinal epithelial cells did not change, while that of TLR 4 and Dectin-1 decreased. Beta-glucan supplementation caused an increase in the expression of TLR 5 and Dectin-1 with no changes in the expression of Caspase-3 and LC3B. After 7 days, a high expression of Caspase-3 was observed in the colitis-induced animals without any changes in the expression of LC3B and TLRs, and simultaneously, a decrease in Dectin-1 expression was observed. The consumption of feed with βGl or βGh resulted in a decrease in Caspase-3 expression and an increase in TLR 5 expression in the CβGl group, with no change in the expression of LC3B and TLR 4. After 21 days, the expression of Caspase-3 and TLRs was not changed by colitis, while that of LC3B and Dectin-1 was decreased. Feed supplementation with βGh resulted in an increase in the expression of both Caspase-3 and LC3B, while the consumption of feed with βGh and βGl increased Dectin-1 expression. However, regardless of the type of nutritional intervention, the expression of TLRs did not change after 21 days. Conclusions: Dietary intake of βGl and βGh significantly reduced colitis by time-dependent modification of autophagy and apoptosis, with βGI exhibiting a stronger effect on apoptosis and βGh on autophagy. The mechanism of this action may be based on the activation of TLRs and Dectin-1 receptor and depends on the period of exacerbation or remission of CD.