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Chicken Egg Yolk Antibodies as Therapeutics in Enteric Infectious Disease: A Review
Yoshinori Mine,Jennifer Kovacs-Nolan 한국식품영양과학회 2002 Journal of medicinal food Vol.5 No.3
Passive immunization by oral administration of specific antibodies has ben an attractive ap-proach against gastrointestinal (GI) pathogens in both humans and animals. Recently, layingchickens have attracted considerable attention as an alternative source of antibodies for theprevention and treatment of infectious GI diseases. After immunization, the specific anti-bodies (called IgY) are transported to the egg yolk, from which the IgY then can be separatedwithout sacrificing chickens. A chicken usually lays about 280 eggs in a year, and egg yolkcontains 10 150 mg of IgY per yolk, suggesting that more than 40 g of IgY per year can beobtained from each chicken through eggs. IgY is also an alternative to antibiotics for treat-ment of enteric antibiotic-resistant pathogens. Oral administration of IgY has proved suc-cessful for treatment of a variety of GI infections, such as bovine and human rotaviruses,bovine coronavirus, Yersinia ruckeri, enterotoxigenic Escherichia coli , Salmonella spp., Ed-wardsiella tarda, Staphylococcus , and Pseudomonas . The IgY technology offers great futureoportunities for designing prophylactic strategies against infectious GI diseases in humansand animals. However, there is still controversy regarding the stability of IgY through the GItract. Finding an effective way to protect the antibodies from degradation in the GI tract wouldopen the door for significant advances in IgY technology and nutraceutical aplications.159
Reduction of Interlukin-8 by Peptides from Digestive Enzyme Hydrolysis of Hen Egg Lysozyme
Mooha Lee,Denise Young,Yoshinori Mine,Cheorun Jo 한국식품과학회 2009 Food Science and Biotechnology Vol.18 No.3
Lysozyme was treated with digestive enzymes and the production of interleukin 8 (IL-8) was measured in Caco-2 cell with the peptides from lysozyme upon stimulating with lipopolysaccharide (LPS) to investigate the overall antiinflammatory activity of lysozyme when it is in digestive tracts. Lysozyme reduced IL-8 production, and the peptides from pepsin hydrolysis of lysozyme had the similar effect. The products of trypsin digestion of lysozyme had no effect on the reduction of IL-8 production while those of pepsin-trypsin hydrolysis did. The effectiveness of lowering IL-8 production was not different by time of the peptide addition. When Caco-2 cells were pre-incubated with peptides for 24 hr, the reduction effects were observed from the peptides from pepsin hydrolysis, indicating that some of the peptides are still remaining in the cells. Therefore, it can be concluded that the IL-8 reduction effect of lysozyme against LPS still remained even after the pepsin and trypsin hydrolysis.
곽수진,김추숙,최명숙,박태선,성미경,윤종원,유훈,Yoshinori Mine,유리나 한국식품영양과학회 2016 Journal of medicinal food Vol.19 No.7
Obesity-induced adipose inflammation plays a crucial role in the development of obesity-induced metabolic disorders such as insulin resistance and type 2 diabetes. In the presence of obesity, hypertrophic adipocytes release inflammatory mediators, including tumor necrosis factor-alpha (TNFα) and monocyte chemoattractant protein-1 (MCP-1), which enhance the recruitment and activation of macrophages, and in turn augment adipose inflammation. We demonstrate that the soy peptide Phe–Leu–Val (FLV) reduces inflammatory responses and insulin resistance in mature adipocytes. Specifically, the soy peptide FLV inhibits the release of inflammatory cytokines (TNFα, MCP-1, and IL-6) from both TNFα-stimulated adipocytes and cocultured adipocytes/macrophages. This inhibition is mediated by the inactivation of the inflammatory signaling molecules c-Jun N-terminal kinase (JNK) and IκB kinase (IKK), and the downregulation of IκBα in the adipocytes. In addition, soy peptide FLV enhances insulin responsiveness and increases glucose uptake in adipocytes. More importantly, we, for the first time, found that adipocytes express peptide transporter 2 (PepT2) protein, and the beneficial action of the soy peptide FLV was disrupted by the peptide transporter inhibitor GlySar. These findings suggest that soy peptide FLV is transported into adipocytes by PepT2 and then downregulates TNFα-induced inflammatory signaling, thereby increasing insulin responsiveness in the cells. The soy peptide FLV, therefore, has the potential to prevent obesity-induced adipose inflammation and insulin resistance.