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Liancheng Lei,Xiaojing Xia,Yanyi Che,Yuanyuan Gao,Shuang Zhao,Changjin Ao,Hongjian Yang,Juxiong Liu,Guo-wen Liu,Wenyu Han,Yuping Wang 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.5
During the lactation cycle of the bovine mammary gland, autophagy is induced in bovine mammary epithelial cells (BMECs) as a cellular homeostasis and survival mecha-nism. Interferon gamma (IFN-) is an important antiproliferative and apoptogenic factor that has been shown to induce autophagy in multiple cell lines in vitro. However, it remains unclear whether IFN- can induce autophagy and whether autophagy affects milk synthesis in BMECs. To understand whether IFN- affects milk synthesis, we isolated and purified primary BMECs and investigated the effect of IFN- on milk synthesis in primary BMECs in vitro. The results showed that IFN- significantly inhibits milk synthesis and that autophagy was clearly induced in primary BMECs in vitro within 24 h. Interestingly, autophagy was observed following IFN- treatment, and the inhibition of autophagy can improve milk protein and milk fat syn-thesis. Conversely, upregulation of autophagy decreased milk synthesis. Furthermore, mechanistic analysis con-firmed that IFN- mediated autophagy by depleting argi-nine and inhibiting the general control nonderepressible-2 kinase (GCN2)/eukaryotic initiation factor 2 (eIF2) signaling pathway in BMECs. Then, it was found that arginine supplementation could attenuate IFN--induced autophagy and recover milk synthesis to some extent. These findings may not only provide a novel measure for preventing the IFN--induced decrease in milk quality but also a useful therapeutic approach for IFN--associated breast diseases in other animals and humans.
( Hongtao Liu ),( Seng Zhu ),( Yingying Sun ),( Na Li ),( Jingmin Gu ),( Changjiang Sun ),( Xin Feng ),( Wenyu Han ),( Jianxia Jiang ),( Liancheng Lei ) 한국미생물 · 생명공학회 2017 Journal of microbiology and biotechnology Vol.27 No.1
Meningitis caused by Streptococcus suis serotype 2 (S. suis 2) is a great threat to the pig industry and human health. Virulence factors associated with the pathogenesis of meningitis have yet to be clearly defined, even though many potential S. suis 2 virulence factors have been identified. This greatly hinders the progress of S. suis 2 meningitis pathogenesis research. In this study, a co-culture blood-brain barrier (BBB) model was established using primary porcine brain microvascular endothelial cells and astrocytes, and the whole genome library of S. suis 2 was constructed using phage display technology. Finally, a total of 14 potential virulence factors contributing to S. suis 2 adherence to and invasion of the BBB were selected by analyzing the interactions between the phage library and the co-culture model. Twelve of these factors have not been previously reported in meningitis-related research. The data provide valuable insight into the pathogenesis of S. suis 2 meningitis and potential targets for the development of drug therapies.
Shuang Wang,Jingmin Gu,Meng Lv,Zhimin Guo,Guangmou Yan,Ling Yu,Chongtao Du,Xin Feng,Wenyu Han,Changjiang Sun,Liancheng Lei 한국미생물학회 2017 The journal of microbiology Vol.55 No.5
Bacteriophage endolysin is one of the most promising antibioticsubstitutes, but in Gram-negative bacteria, the outermembrane prevents the lysin from hydrolyzing peptidoglycansand blocks the development of lysin applications. Theprime strategy for new antibiotic substitutes is allowing lysinto access the peptidoglycan from outside of the bacteria byreformation of the lysin. In this study, the novel Escherichiacoli (E. coli) phage lyase lysep3, which lacks outside-in catalyticability, was fused with the N-terminal region of theBacillus amyloliquefaciens lysin including its cell wall bindingdomain D8 through the best manner of protein fusionbased on the predicted tertiary structure of lysep3-D8 to obtainan engineered lysin that can lyse bacteria from the outside. Our results showed that lysep3-D8 could lyse both Gramnegativeand Gram-positive bacteria, whereas lysep3 and D8have no impact on bacterial growth. The MIC of lysep3-D8on E. coli CVCC1418 is 60 μg/ml; lysep3-D8 can inhibit thegrowth of bacteria up to 12 h at this concentration. The bactericidalspectrum of lysep3-D8 is broad, as it can lyse of allof 14 E. coli strains, 3 P. aeruginosa strains, 1 Acinetobacterbaumannii strain, and 1 Streptococcus strain. Lysep3-D8 hassufficient bactericidal effects on the 14 E. coli strains testedat the concentration of 100 μg/ml. The cell wall binding domainof the engineered lysin can destroy the integrity of theouter membrane of bacteria, thus allowing the catalytic domainto reach its target, peptidoglycan, to lyse the bacteria. Lysep3-D8 can be used as a preservative in fodder to benefitthe health of animals. The method we used here proved to bea successful exploration of the reformation of phage lysin.
Xia, Xiaojing,Che, Yanyi,Gao, Yuanyuan,Zhao, Shuang,Ao, Changjin,Yang, Hongjian,Liu, Juxiong,Liu, Guowen,Han, Wenyu,Wang, Yuping,Lei, Liancheng Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.5
During the lactation cycle of the bovine mammary gland, autophagy is induced in bovine mammary epithelial cells (BMECs) as a cellular homeostasis and survival mechanism. Interferon gamma ($IFN-{\gamma}$) is an important antiproliferative and apoptogenic factor that has been shown to induce autophagy in multiple cell lines in vitro. However, it remains unclear whether $IFN-{\gamma}$ can induce autophagy and whether autophagy affects milk synthesis in BMECs. To understand whether $IFN-{\gamma}$ affects milk synthesis, we isolated and purified primary BMECs and investigated the effect of $IFN-{\gamma}$ on milk synthesis in primary BMECs in vitro. The results showed that $IFN-{\gamma}$ significantly inhibits milk synthesis and that autophagy was clearly induced in primary BMECs in vitro within 24 h. Interestingly, autophagy was observed following $IFN-{\gamma}$ treatment, and the inhibition of autophagy can improve milk protein and milk fat synthesis. Conversely, upregulation of autophagy decreased milk synthesis. Furthermore, mechanistic analysis confirmed that $IFN-{\gamma}$ mediated autophagy by depleting arginine and inhibiting the general control nonderepressible-2 kinase (GCN2)/eukaryotic initiation factor $2{\alpha}$ ($eIF2{\alpha}$) signaling pathway in BMECs. Then, it was found that arginine supplementation could attenuate $IFN-{\gamma}$-induced autophagy and recover milk synthesis to some extent. These findings may not only provide a novel measure for preventing the $IFN-{\gamma}$-induced decrease in milk quality but also a useful therapeutic approach for $IFN-{\gamma}$-associated breast diseases in other animals and humans.