Cronobacter spp. has strong resistance to desiccation and high permeability in Enterobacteriaceae, and powdered infant formula (PIF) is one of the main contamination routes. In recent years, the contamination of Cronobacter spp. in PIF incidents occur from time to time, causing infant serious diseases or death. In this investigation, matrix-assisted laser desorption/ionization time of flight mass spectrometry was used to identify the phenotypes of 35 Cronobacter strains isolated from PIF and its processing environment. Subsequently, the isolates were evaluated for drying and osmotic pressure tolerance. The results showed that the deactivation rate of the strains ranged from 9.01% to 77.57%, and the highest osmotic pressure condition the strains could tolerate was 6% NaCl. In addition, there was a positive correlation between biofilm formation ability and desiccation resistance. Combined with transcriptomics, Cronobacter spp. can activate biofilm synthesis, produce more trehalose, accumulate betaine and electrolytes to stabilize intracellular structure under the two treatment conditions. 31 and 43 genes were found related to desiccation and permeability resistance, respectively. And some genes (cysM, thuF, ycjO, et al) were found to be associated with two tolerances for the first time.

Branched-chain fatty acids (BCFAs) are new bioactive fatty acids with anti-inflammatory properties. However, the role of BCFAs in alleviating ulcerative colitis has not been clarified. Herein, we evaluated the protective effect of BCFAs from goat milk in mice with colitis induced using dextran sodium sulfate and explore the corresponding mechanism. These results show that BCFAs extracted from goat milk can significantly alleviate weight loss in mice, and reduce the disease activity index and the activity of myeloperoxidase while increasing the content of antioxidant enzymes in colon tissue and reducing the oxidation stress response. These data also show that BCFAs can down-regulate the gene and protein expression of the Toll-like receptor 4 (TLR4)/ nuclear factor kappa-B p65 (NF-κB p65)/NOD-like receptor thermal protein domain associated protein 3 (NLRP3) signaling pathway, and at the same time significantly reduce the expression of pro-inflammatory factors Tumor Necrosis Factor Alpha (TNF-α), Interleukin 1β (IL-1β), and Interleukin 18 (IL-18) in colon tissue, and significantly increase the expression of the anti-inflammatory factor Interleukin 10 (IL-10). In conclusion, these results demonstrated that BCFAs in goat milk exerted effects on colitis-related inflammatory cytokines and inhibited inflammation by inducing the TLR4/NF-κB/NLRP3 pathway to alleviate dextran sodium sulfate (DSS)-induced ulcerative colitis. This study provides evidence for the potential of BCFAs as bioactive fatty acids in food products and to ameliorate ulcerative colitis development in mice.

Oxidative stress is one of the main ways to cause alcohol-induced liver injury, and alcoholic liver disease (ALD) has been a common health problem worldwide. Lactic acid bacteria (LAB) is also considered as a potential treatment to alleviate alcohol-induced liver injury. L. plantarum J26 is a LAB isolated from Chinese traditional fermented dairy products with excellent probiotic effects. This study aimed to establish a mice model of alcoholic liver injury through acute-on-chronic alcohol feeding and to study the alleviating effect of pre-intake of L. plantarum J26 on alcohol-induced oxidative liver injury and focus on its potential mechanism of alleviating effect. The results showed that pre-intake of L. plantarum J26 could improve liver pathological changes, reduce lipid accumulation, increase mitochondrial ATP and mitochondrial (mtDNA) levels, and alleviate liver injury. In addition, pre-intake L. plantarum J26 can improve the level of short-chain fatty acids (SCFAs) in the intestines in mice, short chain fatty acids can be used as a signaling molecule activation of nuclear factor E2-related factor 2 (Nrf2) signaling pathway to alleviate liver oxidative stress, and maintain mitochondrial homeostasis by regulating the expression of genes related to mitochondrial dynamics and autophagy, thereby reducing cell apoptosis to alleviate alcohol-induced oxidative liver injury.