AIM:To investigate the role of α-fetoprotein(AFP),a cancer-associated fetal glycoprotein,in glucocorticoidinduced precocious maturation in rat colon.METHODS:Colons from suckling Sprague-Dawley rats were used in this ...AIM:To investigate the role of α-fetoprotein(AFP),a cancer-associated fetal glycoprotein,in glucocorticoidinduced precocious maturation in rat colon.METHODS:Colons from suckling Sprague-Dawley rats were used in this study.Corticosterone acetate at a dose of 100 μg/g body weight was given to normal pups on days 7,9 and 11 after birth to induce hypercorticoidism.Control animals were injected with identical volumes of normal saline.Some rats receiving corticosterone 7 d after birth were also treated with mifepristone(RU38486),a glucocorticoid cytoplasm receptor antagonist to investigate the effects of glucocorticoids(GCs).The morphological changes of the crypt depth and villous height of the villous zone in colon were observed as indicesof colon maturation.Expression levels of AFP in colons were detected by reverse transcriptase polymerase chain reaction and Western blotting.To identify the cellular localization of AFP in developing rat colons,double-immunofluorescent staining was performed using antibodies to specific mesenchymal cell marker and AFP.RESULTS:Corticosterone increased the crypt depth and villous height in the colon of 8-and 10-d-old rats with hypercorticoidism compared with that in the control animals(120% in 8-d-old rats and 118% in 10-d-old rats in villous height,P = 0.021;145% in 8-d-old rats and 124% in 10-d-old rats in crypt depth,P = 0.017).These increases were accompanied by an increase of AFP expression in both mRNA and protein(2.5-folds in 8-dold and 2.5-folds in 10-d-old rats higher than in control animals,P = 0.035;1.8-folds in 8-d-old and 1.3-folds in 10-d-old rats higher than in control animals,P = 0.023).Increased crypt depth and villous height and increased expression of AFP in the colon of rats with hypercorticoidism were blocked by mifepristone.Both had positive staining for AFP or vimentin,and overlapped in mesenchymal cells at each tested colon.CONCLUSION:GCs promote the development of rat colon.AFP appears to be involved,in part,in mediating the effects of GCs in the developmental colon.展开更多
Four kinds of antifungal compounds from an extract of Paenibacillus polymyxa A21 with molecular masses of 883.56, 897.59, 947.55, and 961.58 Da were characterized as the members of fusaricidin-type of antibiotics acco...Four kinds of antifungal compounds from an extract of Paenibacillus polymyxa A21 with molecular masses of 883.56, 897.59, 947.55, and 961.58 Da were characterized as the members of fusaricidin-type of antibiotics according to LC-MS analysis. Fusaricidins isolated from culture filtrate displayed high antagonistic activity against several plant fungal pathogens, especially Botrytis cinerea, the causal agent of gray mold. The fusaricidins biosynthetic gene cluster(BGC) from A21 was cloned by PCR and comparative cluster analysis revealed that gene fus TE, the 3′ boundary of the fusaricidin BGC in strain PKB1, was not present in fusaricidin BGC of A21, indicating that fus TE is not necessary for fusaricidin synthesis. Fusaricidin extract from A21 significantly reduced gray mold disease incidence and severity on tomato. The m RNA levels for three pathogenesis-related proteins(PRs) revealed that treatment of tomato leaves with fusaricidin extract induced the expression of PR genes to different levels, suggesting that one reason for the reduction of gray mold infection by fusaricidin is induction of PR proteins, which lead to increased resistance to pathogens. This is the first report of the application of fusaricidins to control tomato gray mold and the comparative cluster analysis provides important molecular basis for research on fusaricidin biosynthesis.展开更多
Cystic echinococcosis,which is caused by larval infection of Echinococcus granulosus(E.granulosus)sensu lato,is a widespread chronic cyst-forming helminthic disease that affects up to 3 million people.1 E.granulosus c...Cystic echinococcosis,which is caused by larval infection of Echinococcus granulosus(E.granulosus)sensu lato,is a widespread chronic cyst-forming helminthic disease that affects up to 3 million people.1 E.granulosus can actively divert the host immune response towards anergy and anti-inflammatory pathways.2 Previous studies have shown that E.granulosus can escape host immunosurveillance by modulating the maturation of dendritic cells(DCs).3,4 Nevertheless,how E.granulosus,an extracellular pathogen,modulates the inflammatory response in DCs remains poorly understood.In this study,we investigated the effects of E.granulosus cyst fluid(EgCF)on bone marrow-derived DCs(BMDCs)exposed to LPS,an inflammatory stimulus,and the mechanisms involved in the EgCF–DCs immune modulation.展开更多
Dear Editor,Human immunodeficiency virus type 1(HIV-1)infection is mainly initiated on mucosal epithelial surfaces.Exposure to HIV-1 impairs the mucosal epithelial barrier,allowing viral transmission across the mucosa...Dear Editor,Human immunodeficiency virus type 1(HIV-1)infection is mainly initiated on mucosal epithelial surfaces.Exposure to HIV-1 impairs the mucosal epithelial barrier,allowing viral transmission across the mucosal epithelium.1 Interaction of HIV-1 envelope glycoprotein gp120 with its primary receptor,cluster of differentiation 4(CD4),and chemokine coreceptors has been implicated in the disruption of epithelial cell junctions upon HIV-1 exposure.1 However,the molecular details and underlying mechanisms of this disruption remain elusive.展开更多
文摘AIM:To investigate the role of α-fetoprotein(AFP),a cancer-associated fetal glycoprotein,in glucocorticoidinduced precocious maturation in rat colon.METHODS:Colons from suckling Sprague-Dawley rats were used in this study.Corticosterone acetate at a dose of 100 μg/g body weight was given to normal pups on days 7,9 and 11 after birth to induce hypercorticoidism.Control animals were injected with identical volumes of normal saline.Some rats receiving corticosterone 7 d after birth were also treated with mifepristone(RU38486),a glucocorticoid cytoplasm receptor antagonist to investigate the effects of glucocorticoids(GCs).The morphological changes of the crypt depth and villous height of the villous zone in colon were observed as indicesof colon maturation.Expression levels of AFP in colons were detected by reverse transcriptase polymerase chain reaction and Western blotting.To identify the cellular localization of AFP in developing rat colons,double-immunofluorescent staining was performed using antibodies to specific mesenchymal cell marker and AFP.RESULTS:Corticosterone increased the crypt depth and villous height in the colon of 8-and 10-d-old rats with hypercorticoidism compared with that in the control animals(120% in 8-d-old rats and 118% in 10-d-old rats in villous height,P = 0.021;145% in 8-d-old rats and 124% in 10-d-old rats in crypt depth,P = 0.017).These increases were accompanied by an increase of AFP expression in both mRNA and protein(2.5-folds in 8-dold and 2.5-folds in 10-d-old rats higher than in control animals,P = 0.035;1.8-folds in 8-d-old and 1.3-folds in 10-d-old rats higher than in control animals,P = 0.023).Increased crypt depth and villous height and increased expression of AFP in the colon of rats with hypercorticoidism were blocked by mifepristone.Both had positive staining for AFP or vimentin,and overlapped in mesenchymal cells at each tested colon.CONCLUSION:GCs promote the development of rat colon.AFP appears to be involved,in part,in mediating the effects of GCs in the developmental colon.
基金supported by the Scientific and Technological Innovation Capacity Construction Special Funds, Beijing Academy of Agriculture and Forestry (KJCX20170410)the Science and Technology Innovation Fund from the Beijing Academy of Agriculture and Forestry Sciences (QNJJ201519)Beijing Key Laboratory of Environment Friendly Management on Fruit Diseases and Pests in North China (BZ0432)
文摘Four kinds of antifungal compounds from an extract of Paenibacillus polymyxa A21 with molecular masses of 883.56, 897.59, 947.55, and 961.58 Da were characterized as the members of fusaricidin-type of antibiotics according to LC-MS analysis. Fusaricidins isolated from culture filtrate displayed high antagonistic activity against several plant fungal pathogens, especially Botrytis cinerea, the causal agent of gray mold. The fusaricidins biosynthetic gene cluster(BGC) from A21 was cloned by PCR and comparative cluster analysis revealed that gene fus TE, the 3′ boundary of the fusaricidin BGC in strain PKB1, was not present in fusaricidin BGC of A21, indicating that fus TE is not necessary for fusaricidin synthesis. Fusaricidin extract from A21 significantly reduced gray mold disease incidence and severity on tomato. The m RNA levels for three pathogenesis-related proteins(PRs) revealed that treatment of tomato leaves with fusaricidin extract induced the expression of PR genes to different levels, suggesting that one reason for the reduction of gray mold infection by fusaricidin is induction of PR proteins, which lead to increased resistance to pathogens. This is the first report of the application of fusaricidins to control tomato gray mold and the comparative cluster analysis provides important molecular basis for research on fusaricidin biosynthesis.
基金supported by the National Natural Science Foundation of China(81760371,81760570,81602810,81703174)the XPCC Youth Science and Technology Innovation Leading Talent Program(2018CB017)Key Areas of Science and Technology Projects(2019AB031).
文摘Cystic echinococcosis,which is caused by larval infection of Echinococcus granulosus(E.granulosus)sensu lato,is a widespread chronic cyst-forming helminthic disease that affects up to 3 million people.1 E.granulosus can actively divert the host immune response towards anergy and anti-inflammatory pathways.2 Previous studies have shown that E.granulosus can escape host immunosurveillance by modulating the maturation of dendritic cells(DCs).3,4 Nevertheless,how E.granulosus,an extracellular pathogen,modulates the inflammatory response in DCs remains poorly understood.In this study,we investigated the effects of E.granulosus cyst fluid(EgCF)on bone marrow-derived DCs(BMDCs)exposed to LPS,an inflammatory stimulus,and the mechanisms involved in the EgCF–DCs immune modulation.
基金supported by grants from the National Natural Science Foundation of China(31471262,31701209,and 31771542).
文摘Dear Editor,Human immunodeficiency virus type 1(HIV-1)infection is mainly initiated on mucosal epithelial surfaces.Exposure to HIV-1 impairs the mucosal epithelial barrier,allowing viral transmission across the mucosal epithelium.1 Interaction of HIV-1 envelope glycoprotein gp120 with its primary receptor,cluster of differentiation 4(CD4),and chemokine coreceptors has been implicated in the disruption of epithelial cell junctions upon HIV-1 exposure.1 However,the molecular details and underlying mechanisms of this disruption remain elusive.
