Bovine leukemia virus (BLV) is a retrovirus that causes enzootic bovine leucosis (EBL), which is the most significant neoplastic disease in cattle. Although EBL has been successfully eradicated in most European countries, infections continue to rise in Argentina, Brazil, Canada, Japan, and the United States. BLV imposes a substantial economic burden on the cattle industry, particularly in dairy farming, as it leads to a decline in animal production performance and increases the risk of disease. Moreover, trade restrictions on diseased animals and products between countries and regions further exacerbate the problem. Recent studies have also identified fragments of BLV nucleic acid in human breast cancer tissues, raising concerns for public health. Due to the absence of an effective vaccine, controlling the disease is challenging. Therefore, it is crucial to accurately detect and diagnose BLV at an early stage to control its spread and minimize economic losses. This review provides a comprehensive examination of BLV, encompassing its genomic structure, epidemiology, modes of transmission, clinical symptoms, detection methods, hazards, and control strategies. The aim is to provide strategic information for future BLV research.

Astragalus membranaceus (Fisch.) Bunge is one of the most widely used traditional Chinese herbal medicines. It is used as immune stimulant, tonic, antioxidant, hepatoprotectant, diuretic, antidiabetic, anticancer, and expectorant. The purpose of the study was to investigate the curative effects of the decoction obtained from Astragalus membranaceus root in intestinal mucosal injury induced by LPS in mice. An LPS-induced intestinal mucosal injury mice model was applied in the study. The mice were post-treated with Astragalus membranaceus decoction (AMD) for 4 days after 3 days LPS induction. ELISA kit was used to detect the content of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-4,IL-6 and IL-8 in the serum of each group mice. The morphological changes in intestinal mucosa at the end of the experiments were observed. Both VH (villus height) and CD (crypt depth) were measured using H&E-stained sections. There were significant differences in IL-1β, IL-4,IL-6, IL-8 and TNF-α levels in AMD-treated group on the 7th day compared to the controls group. The VH was lower in duodenum, jejunum and the ileum in LPS-treated mice compared to the control animals. Similarly, there was also decrease in V/C. Compared to the control mice, for AMD-treated mice, VH and CD had no significantly differences. Astragalus membranaceus reduced intestinal mucosal damage and promoted tissue repair by inhibiting the expression of inflammatory cytokine.

Selenium (Se) is an important nutritional trace element possessing antioxidant properties. Our goal was to elucidate the effect and mechanism of Se deficiency on the intestinal cell fate. One-day-old three-yellow chickens were fed a low Se diet for 1, 3, and 5 weeks. Histologic characteristics, protein expression profiles, antioxidant activities, inflammatory signaling, and the apoptosis status in duodenum mucosa were investigated. Histological results showed that Se deficiency could increase inflammatory cell infiltration, karyopyknosis of the epithelial cells, cytoplasm vacuolization and dissolution of goblet cells. The proteomics results indicated that Se deficiency could induce apoptosis of cells in duodenal villi via inhibition of antioxidant redox signaling and activation of NF-κB signaling. Further analysis results showed that Se deficiency decreased the total antioxidant capacity of duodenum mucosa via down-regulating the transcription level and activities of glutathione peroxidase (GPX), reduced glutathione (GSH), and thioredoxin reductase (TrxR). The NF-κB signaling pathway was activated by Se deficiency-induced reactive oxygen species (ROS). TUNEL, DNA ladder, immunohistochemical assay, and western blotting proved that selenium deficiency could induce duodenal villi cell apoptosis. The results also indicated that Se deficiency can cause duodenal villi cell apoptosis via an oxidative stress-induced mitochondrial apoptosis pathway (intrinsic pathway) and an inflammatory signaling-induced death receptor pathway (extrinsic pathway). Our data may provide new insight into the prevention and treatment of chronic diarrhea caused by Se deficiency.

Background: Staphylococcus aureus is the causative agent of chronic mastitis, and can form a biofilm that is difficult to completely remove once formed. Disinfectants are effective against S. aureus, but their activity is easily affected by environmental factors and they are corrosive to equipment and chemically toxic to livestock and humans. Therefore, we investigated the potential utility of a bacteriophage as a narrow-spectrum disinfectant against biofilms formed by S. aureus. In this study, we isolated and characterized bacteriophage vB_SauM_SDQ (abbreviated to SDQ) to determine its efficacy in removing S. aureus biofilms. Results: SDQ belongs to the family Myoviridae and consists of a hexagonal head, long neck, and short tail. This phage can sterilize a 10⁹ CFU/mL culture of S. aureus in 12 h and multiply itself 1000-fold in that time. Biofilms formed on polystyrene, milk, and mammary-gland tissue were significantly reduced after SDQ treatment. Fluorescence microscopy and scanning electron microscopy showed that SDQ destroyed the biofilm structure. Moreover, the titer of SDQ remained relatively high after the lysis of the bacteria and the removal of the biofilm, exerting a continuous bacteriostatic effect. SDQ also retained its full activity under conditions that mimic common environments, i.e., in the presence of nonionic detergents, tap water, or organic materials. A nonionic detergent (Triton X-100) enhanced the removal of biofilm by SDQ. Conclusions: Our results suggest that SDQ, a specific lytic S. aureus phage, can be used to control biofilm infections. SDQ maintains its full activity in the presence of nonionic detergents, tap water, metal chelators, and organic materials, and can be used in combination with detergents. We propose this phage as a narrow-spectrum disinfectant against S. aureus, to augment or supplement the use of broad-spectrum disinfectants in the prevention and control of the mastitis and dairy industry contamination caused by S. aureus.

Sterol regulatory element binding protein 1 (SREBP1) has a central regulatory effect on milk fat synthesis. Lipopolysaccharides (LPS) can induce mastitis and cause milk fat depression in cows. SREBP1 is also known to be associated with inflammatory regulation. Thus, in the current study, we hypothesized that LPS-induced milk fat depression in dairy cow mammary epithelial cells (DCMECs) operates via decreased SREBP1 expression and activity. To examine the hypothesis, DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS (10 µg/ml). LPS treatment of DCMECs suppressed lipid-metabolism-related transcription factor SREBP1 mRNA expression, nuclear translocation and protein expression, leading to reduced triglyceride content. The transcription levels of acetyl-CoA carboxylase-1 and fatty acid synthetase were significantly down-regulated in DCMECs after LPS treatment, suggesting that acetyl-CoA carboxylase-1 and fatty acid synthetase involved in de novo milk fat synthesis was regulated by SREBP1. In summary, these results suggest that LPS induces milk fat depression in dairy cow mammary epithelial cells via decreased expression of SREBP1 in a time-dependent manner.