Food and gut originated bacteriocins involved in gut microbe-host interactions.

The gut microbes interact with each other as well as host, influencing human health and some diseases. Many gut commensals and food originated bacteria produce bacteriocins which can inhibit pathogens and modulate gut microbiota. Bacteriocins have comparable narrow antimicrobial spectrum and are attractive potentials for precision therapy of gut disorders. In this review, the bacteriocins from food and gut microbiomes and their involvement in the interaction between producers and gut ecosystem, along with their characteristics, types, biosynthesis, and functions are described and discussed. Bacteriocins are produced by many intestinal commensals and food microbes among which lactic acid bacteria (many are probiotics) has been paid more attention. Bacteriocin production has been generally regarded as a probiotic trait. They give a competitive advantage to bacteria, enabling their colonization in human gut, and mediating the interaction between the producers and host ecosystem. They fight against unwanted bacteria and pathogens without significant impact on the composition of commensal microbiota. Bacteriocins assist the producers to survive and colonize in the gut microbial populations. There is a great need to evaluate and utilize the potential of bacteriocins for improved therapeutic implications for intestinal health.

Nisin Z attenuates lipopolysaccharide-induced mastitis by inhibiting the ERK1/2 and p38 mitogen-activated protein kinase signaling pathways.

Nisin Z is a possible alternative for treating bovine mastitis by inhibiting mastitis-causing pathogens and having anti-inflammatory activity. However, the anti-inflammatory mechanism of nisin Z on mastitis is unknown. Our study aimed to investigate the mechanisms of nisin Z on mastitis. Our results showed that nisin Z inhibited the activation of the ERK1/2 and p38 mitogen-activated protein kinase (MAPK) signaling pathway, decreased the release of pro-inflammatory cytokines (i.e., tumor necrosis factor-α, IL-1ß, and IL-6), and increased the anti-inflammatory cytokine (IL-10) in lipopolysaccharide (LPS)-induced MCF10A cells. After intraperitoneal injection, nisin Z significantly decreased inflammatory cell infiltration in the mammary gland, as well as decreased myeloperoxidase and pro-inflammatory cytokines in serum and mammary gland. Western blot analysis revealed that nisin Z also dramatically suppressed the activation of the ERK1/2 and p38 MAPK signaling pathways in LPS-induced mastitis mice. We also found that nisin Z treatment could enhance the blood-milk barrier. In summary, our study demonstrated that nisin Z exerted an anti-inflammatory effect by inhibiting the ERK1/2 and p38 MAPK signaling pathway and promoting the blood-milk barrier on LPS-induced mastitis.

Exploring the bacterial community succession and metabolic profiles of Lonicera japonica Thunb. residues during anaerobic fermentation.

Discarding Lonicera japonica Thunb. (LJT) residues containing many active metabolites create tremendous waste. This study aimed to effectively use LJT residues by anaerobic fermentation. Fermentation significantly decreased the pH values and reduced the abundance of undesirable bacteria (potential pathogenic and biofilm-forming) while increasing Lactobacillus abundance. Compound additive use further improved fermentation quality (significantly increased the lactic acid (LA) content and decreased the pH values and ammonia nitrogen (a-N) content) and nutrient quality (significantly decreased the acid detergent fiber (ADF) content and increased the water-soluble carbohydrate (WSC) content) and optimized the microbial community (increased the Lactobacillus abundance). Fermentation also altered the flavonoids, alkaloids and phenols contents in the residues with minor effects on the functional metabolites amounts. The LJT residues metabolic profile was mainly attributed to its epiphytic bacteria, with a small contribution from the compound additive. Thus, compound additives may improve anaerobic LJT residue fermentation without functionally impairing the metabolites.