cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.12852009.v1
title: Maltose promotes crucian carp survival against <i>Aeromonas sobrial</i> infection at high temperature

description: Temperature influences fish’s susceptibility to infectious disease through an immune response. However, the mechanism underlying this regulation is yet to be elucidated. In this study, we compared the susceptibility of crucian carp that were grown at 18°C and 33°C, respectively, to <i>Aeromonas sobrial</i> infection and found that crucian carp was more susceptible when grown at 33°C. These distinct susceptibilities of fish at different temperatures to infection may partially be explained by their differences in the metabolism as revealed by comparative metabolomics profiling: crucian carp demonstrated enhanced TCA cycle but reduced fatty acid biosynthesis; Our study also found that maltose was the most suppressed metabolite in fish grown at 33°C. Importantly, exogenous injection of maltose enhances crucian carp survival grown at 33°C by 30%. Further study showed that exogenous maltose downregulated the production of several cytokines but enhanced the lysozyme (<i>lyz</i>) and complement component <i>c3</i>, which involves the humoral innate immunity. Our results suggest that maltose promotes the survival of crucian carp likely through fine tuning the immune gene expression, and this finding provides a novel approach to manage bacterial infection.
DOI: 10.6084/m9.figshare.12852009.v2
title: Maltose promotes crucian carp survival against <i>Aeromonas sobrial</i> infection at high temperature

description: Temperature influences fish’s susceptibility to infectious disease through an immune response. However, the mechanism underlying this regulation is yet to be elucidated. In this study, we compared the susceptibility of crucian carp that were grown at 18°C and 33°C, respectively, to <i>Aeromonas sobrial</i> infection and found that crucian carp was more susceptible when grown at 33°C. These distinct susceptibilities of fish at different temperatures to infection may partially be explained by their differences in the metabolism as revealed by comparative metabolomics profiling: crucian carp demonstrated enhanced TCA cycle but reduced fatty acid biosynthesis; Our study also found that maltose was the most suppressed metabolite in fish grown at 33°C. Importantly, exogenous injection of maltose enhances crucian carp survival grown at 33°C by 30%. Further study showed that exogenous maltose downregulated the production of several cytokines but enhanced the lysozyme (<i>lyz</i>) and complement component <i>c3</i>, which involves the humoral innate immunity. Our results suggest that maltose promotes the survival of crucian carp likely through fine tuning the immune gene expression, and this finding provides a novel approach to manage bacterial infection.
DOI: 10.6084/m9.figshare.12852009.v3
title: Maltose promotes crucian carp survival against <i>Aeromonas sobrial</i> infection at high temperature

description: Temperature influences fish’s susceptibility to infectious disease through an immune response. However, the mechanism underlying this regulation is yet to be elucidated. In this study, we compared the susceptibility of crucian carp that were grown at 18°C and 33°C, respectively, to <i>Aeromonas sobrial</i> infection and found that crucian carp was more susceptible when grown at 33°C. These distinct susceptibilities of fish at different temperatures to infection may partially be explained by their differences in the metabolism as revealed by comparative metabolomics profiling: crucian carp demonstrated enhanced TCA cycle but reduced fatty acid biosynthesis; Our study also found that maltose was the most suppressed metabolite in fish grown at 33°C. Importantly, exogenous injection of maltose enhances crucian carp survival grown at 33°C by 30%. Further study showed that exogenous maltose downregulated the production of several cytokines but enhanced the lysozyme (<i>lyz</i>) and complement component <i>c3</i>, which involves the humoral innate immunity. Our results suggest that maltose promotes the survival of crucian carp likely through fine tuning the immune gene expression, and this finding provides a novel approach to manage bacterial infection.
DOI: 10.6084/m9.figshare.12852018
title: Establishment of stable Vero cell lines expressing TMPRSS2 and MSPL: A useful tool for propagating porcine epidemic diarrhea virus in the absence of exogenous trypsin

description: Porcine epidemic diarrhea virus (PEDV) is the causative agent of porcine epidemic diarrhea, causing substantial economic losses to the swine industry worldwide. However, the development of PEDV vaccine is hampered by its low propagation titer <i>in vitro</i>, due to difficulty in adapting to the cells and complex culture conditions, even in the presence of trypsin. Furthermore, the frequent variation, recombination, and evolution of PEDV resulted in reemergence and vaccination failure. In this study, we established the Vero/TMPRSS2 and Vero/MSPL cell lines, constitutively expressing type II transmembrane serine protease TMPRSS2 and MSPL, in order to increase the stability and titer of PEDV culture and isolation <i>in vitro</i>. Our study revealed that the Vero/TMPRSS2, especially Vero/MSPL cell lines, can effectively facilitate the titer and multicycle replication of cell-adapted PEDV in the absence of exogenous trypsin, by cleaving and activating PEDV S protein. Furthermore, our results also highlighted that Vero/TMPRSS2 and Vero/MSPL cells can significantly enhance the isolation of PEDV from the clinical tissue samples as well as promote viral infection and replication by cell-cell fusion. The successful construction of the Vero/TMPRSS2 and Vero/MSPL cell lines provides a useful approach for the isolation and propagation of PEDV, simplification of virus culture, and large-scale production of industrial vaccine, and the cell lines are also an important system to research PEDV S protein cleaved by host protease.
DOI: 10.6084/m9.figshare.12852018.v1
title: Establishment of stable Vero cell lines expressing TMPRSS2 and MSPL: A useful tool for propagating porcine epidemic diarrhea virus in the absence of exogenous trypsin

description: Porcine epidemic diarrhea virus (PEDV) is the causative agent of porcine epidemic diarrhea, causing substantial economic losses to the swine industry worldwide. However, the development of PEDV vaccine is hampered by its low propagation titer <i>in vitro</i>, due to difficulty in adapting to the cells and complex culture conditions, even in the presence of trypsin. Furthermore, the frequent variation, recombination, and evolution of PEDV resulted in reemergence and vaccination failure. In this study, we established the Vero/TMPRSS2 and Vero/MSPL cell lines, constitutively expressing type II transmembrane serine protease TMPRSS2 and MSPL, in order to increase the stability and titer of PEDV culture and isolation <i>in vitro</i>. Our study revealed that the Vero/TMPRSS2, especially Vero/MSPL cell lines, can effectively facilitate the titer and multicycle replication of cell-adapted PEDV in the absence of exogenous trypsin, by cleaving and activating PEDV S protein. Furthermore, our results also highlighted that Vero/TMPRSS2 and Vero/MSPL cells can significantly enhance the isolation of PEDV from the clinical tissue samples as well as promote viral infection and replication by cell-cell fusion. The successful construction of the Vero/TMPRSS2 and Vero/MSPL cell lines provides a useful approach for the isolation and propagation of PEDV, simplification of virus culture, and large-scale production of industrial vaccine, and the cell lines are also an important system to research PEDV S protein cleaved by host protease.
DOI: 10.6084/m9.figshare.12852018.v3
title: Establishment of stable Vero cell lines expressing TMPRSS2 and MSPL: A useful tool for propagating porcine epidemic diarrhea virus in the absence of exogenous trypsin

description: Porcine epidemic diarrhea virus (PEDV) is the causative agent of porcine epidemic diarrhea, causing substantial economic losses to the swine industry worldwide. However, the development of PEDV vaccine is hampered by its low propagation titer <i>in vitro</i>, due to difficulty in adapting to the cells and complex culture conditions, even in the presence of trypsin. Furthermore, the frequent variation, recombination, and evolution of PEDV resulted in reemergence and vaccination failure. In this study, we established the Vero/TMPRSS2 and Vero/MSPL cell lines, constitutively expressing type II transmembrane serine protease TMPRSS2 and MSPL, in order to increase the stability and titer of PEDV culture and isolation <i>in vitro</i>. Our study revealed that the Vero/TMPRSS2, especially Vero/MSPL cell lines, can effectively facilitate the titer and multicycle replication of cell-adapted PEDV in the absence of exogenous trypsin, by cleaving and activating PEDV S protein. Furthermore, our results also highlighted that Vero/TMPRSS2 and Vero/MSPL cells can significantly enhance the isolation of PEDV from the clinical tissue samples as well as promote viral infection and replication by cell-cell fusion. The successful construction of the Vero/TMPRSS2 and Vero/MSPL cell lines provides a useful approach for the isolation and propagation of PEDV, simplification of virus culture, and large-scale production of industrial vaccine, and the cell lines are also an important system to research PEDV S protein cleaved by host protease.
DOI: 10.6084/m9.figshare.12852018.v2
title: Establishment of stable Vero cell lines expressing TMPRSS2 and MSPL: A useful tool for propagating porcine epidemic diarrhea virus in the absence of exogenous trypsin

description: Porcine epidemic diarrhea virus (PEDV) is the causative agent of porcine epidemic diarrhea, causing substantial economic losses to the swine industry worldwide. However, the development of PEDV vaccine is hampered by its low propagation titer <i>in vitro</i>, due to difficulty in adapting to the cells and complex culture conditions, even in the presence of trypsin. Furthermore, the frequent variation, recombination, and evolution of PEDV resulted in reemergence and vaccination failure. In this study, we established the Vero/TMPRSS2 and Vero/MSPL cell lines, constitutively expressing type II transmembrane serine protease TMPRSS2 and MSPL, in order to increase the stability and titer of PEDV culture and isolation <i>in vitro</i>. Our study revealed that the Vero/TMPRSS2, especially Vero/MSPL cell lines, can effectively facilitate the titer and multicycle replication of cell-adapted PEDV in the absence of exogenous trypsin, by cleaving and activating PEDV S protein. Furthermore, our results also highlighted that Vero/TMPRSS2 and Vero/MSPL cells can significantly enhance the isolation of PEDV from the clinical tissue samples as well as promote viral infection and replication by cell-cell fusion. The successful construction of the Vero/TMPRSS2 and Vero/MSPL cell lines provides a useful approach for the isolation and propagation of PEDV, simplification of virus culture, and large-scale production of industrial vaccine, and the cell lines are also an important system to research PEDV S protein cleaved by host protease.
DOI: 10.6084/m9.figshare.12852030
title: The interaction between flagellin and the glycosphingolipid Gb3 on host cells contributes to <i>Bacillus cereus</i> acute infection

description: <b>Bacillus cereus</b> is an opportunistic pathogen that can cause emetic or diarrheal foodborne illness. Previous studies have identified multiple pathogenic <i>B. cereus</i> strains and characterized a variety of virulence factors. Here, we demonstrate that the virulence and lethality of <i>B. cereus</i> for mammalian cells and host animals involve the interaction of <i>B. cereus</i> flagellin proteins and the host-cell-surface-localized glycosphingolipid Gb3 (CD77, Galα1-4Galβ1-4Glcβ1-Cer). We initially found that <i>B. cereus</i> infection was less lethal for Gb3-deficiencient <i>A4galt</i><sup>−/-</sup> mice than for wild-type mice. Subsequent experiments established that some factor other than secreted toxins must account of the observed differential lethality: Gb3-deficiencient <i>A4galt</i><sup>−/-</sup> mice were equally susceptible to secreted-virulence-factor-mediated death as WT mice, and we observed no differences in the bacterial loads of spleens or livers of mice treated with <i>B. cereus</i> strain vs. mice infected with a mutant variant of incapable of producing many secreted toxins. A screen for host-interacting <i>B. cereus</i> cell wall components identified the well-known flagellin protein, and both flagellin knockout strain assays and Gb3 inhibitor studies confirmed that flagellin does interact with Gb3 in a manner that affects <i>B. cereus</i> infection of host cells. Finally, we show that treatment with polyclonal antibody against flagellin can protect mice against <i>B. cereus</i> infection. Thus, beyond demonstrating a previously unappreciated interaction between a bacterial motor protein and a mammalian cell wall glycosphingolipid, our study will provide useful information for the development of therapies to treat infection of <i>B. cereus</i>.
DOI: 10.6084/m9.figshare.12852030.v1
title: The interaction between flagellin and the glycosphingolipid Gb3 on host cells contributes to <i>Bacillus cereus</i> acute infection

description: is an opportunistic pathogen that can cause emetic or diarrheal foodborne illness. Previous studies have identified multiple pathogenic <i>B. cereus</i> strains and characterized a variety of virulence factors. Here, we demonstrate that the virulence and lethality of <i>B. cereus</i> for mammalian cells and host animals involve the interaction of <i>B. cereus</i> flagellin proteins and the host-cell-surface-localized glycosphingolipid Gb3 (CD77, Galα1-4Galβ1-4Glcβ1-Cer). We initially found that <i>B. cereus</i> infection was less lethal for Gb3-deficiencient <i>A4galt</i>
 <sup>−/-</sup> mice than for wild-type mice. Subsequent experiments established that some factor other than secreted toxins must account of the observed differential lethality: Gb3-deficiencient <i>A4galt</i>
 <sup>−/-</sup> mice were equally susceptible to secreted-virulence-factor-mediated death as WT mice, and we observed no differences in the bacterial loads of spleens or livers of mice treated with <i>B. cereus</i> strain vs. mice infected with a mutant variant of incapable of producing many secreted toxins. A screen for host-interacting <i>B. cereus</i> cell wall components identified the well-known flagellin protein, and both flagellin knockout strain assays and Gb3 inhibitor studies confirmed that flagellin does interact with Gb3 in a manner that affects <i>B. cereus</i> infection of host cells. Finally, we show that treatment with polyclonal antibody against flagellin can protect mice against <i>B. cereus</i> infection. Thus, beyond demonstrating a previously unappreciated interaction between a bacterial motor protein and a mammalian cell wall glycosphingolipid, our study will provide useful information for the development of therapies to treat infection of <i>B. cereus</i>.
DOI: 10.6084/m9.figshare.12852030.v3
title: The interaction between flagellin and the glycosphingolipid Gb3 on host cells contributes to <i>Bacillus cereus</i> acute infection

description: <b>Bacillus cereus</b> is an opportunistic pathogen that can cause emetic or diarrheal foodborne illness. Previous studies have identified multiple pathogenic <i>B. cereus</i> strains and characterized a variety of virulence factors. Here, we demonstrate that the virulence and lethality of <i>B. cereus</i> for mammalian cells and host animals involve the interaction of <i>B. cereus</i> flagellin proteins and the host-cell-surface-localized glycosphingolipid Gb3 (CD77, Galα1-4Galβ1-4Glcβ1-Cer). We initially found that <i>B. cereus</i> infection was less lethal for Gb3-deficiencient <i>A4galt</i><sup>−/-</sup> mice than for wild-type mice. Subsequent experiments established that some factor other than secreted toxins must account of the observed differential lethality: Gb3-deficiencient <i>A4galt</i><sup>−/-</sup> mice were equally susceptible to secreted-virulence-factor-mediated death as WT mice, and we observed no differences in the bacterial loads of spleens or livers of mice treated with <i>B. cereus</i> strain vs. mice infected with a mutant variant of incapable of producing many secreted toxins. A screen for host-interacting <i>B. cereus</i> cell wall components identified the well-known flagellin protein, and both flagellin knockout strain assays and Gb3 inhibitor studies confirmed that flagellin does interact with Gb3 in a manner that affects <i>B. cereus</i> infection of host cells. Finally, we show that treatment with polyclonal antibody against flagellin can protect mice against <i>B. cereus</i> infection. Thus, beyond demonstrating a previously unappreciated interaction between a bacterial motor protein and a mammalian cell wall glycosphingolipid, our study will provide useful information for the development of therapies to treat infection of <i>B. cereus</i>.
DOI: 10.6084/m9.figshare.12852030.v2
title: The interaction between flagellin and the glycosphingolipid Gb3 on host cells contributes to <i>Bacillus cereus</i> acute infection

description: is an opportunistic pathogen that can cause emetic or diarrheal foodborne illness. Previous studies have identified multiple pathogenic <i>B. cereus</i> strains and characterized a variety of virulence factors. Here, we demonstrate that the virulence and lethality of <i>B. cereus</i> for mammalian cells and host animals involve the interaction of <i>B. cereus</i> flagellin proteins and the host-cell-surface-localized glycosphingolipid Gb3 (CD77, Galα1-4Galβ1-4Glcβ1-Cer). We initially found that <i>B. cereus</i> infection was less lethal for Gb3-deficiencient <i>A4galt</i><sup>−/-</sup> mice than for wild-type mice. Subsequent experiments established that some factor other than secreted toxins must account of the observed differential lethality: Gb3-deficiencient <i>A4galt</i><sup>−/-</sup> mice were equally susceptible to secreted-virulence-factor-mediated death as WT mice, and we observed no differences in the bacterial loads of spleens or livers of mice treated with <i>B. cereus</i> strain vs. mice infected with a mutant variant of incapable of producing many secreted toxins. A screen for host-interacting <i>B. cereus</i> cell wall components identified the well-known flagellin protein, and both flagellin knockout strain assays and Gb3 inhibitor studies confirmed that flagellin does interact with Gb3 in a manner that affects <i>B. cereus</i> infection of host cells. Finally, we show that treatment with polyclonal antibody against flagellin can protect mice against <i>B. cereus</i> infection. Thus, beyond demonstrating a previously unappreciated interaction between a bacterial motor protein and a mammalian cell wall glycosphingolipid, our study will provide useful information for the development of therapies to treat infection of <i>B. cereus</i>.
DOI: 10.6084/m9.figshare.12852033
title: New insights into the evolution of host specificity of three <i>Penicillium</i> species and the pathogenicity of <i>P. Italicum</i> involving the infection of Valencia orange (<i>Citrus sinensis</i>)

description: Blue and green molds, the common phenotypes of post-harvest diseases in fruits, are mainly caused by<i> Penicillium </i>fungal species, including<i> P. italicum, P. digitatum,</i> and <i>P. expansum</i>. We sequenced and assembled the genome of a <i>P. italicum </i>strain, which contains 31,034,623 bp with 361 scaffolds and 627 contigs. The mechanisms underlying the evolution of host specificity among the analyzed <i>Penicillium </i>species were associated with the expansion of protein families, genome restructuring, horizontal gene transfer, and positive selection pressure. A dual-transcriptome analysis following the infection of Valencia orange <i>(Citrus sinensis)</i> by <i>P. italicum </i>resulted in the annotation of 9,307 <i>P. italicum</i> genes and 24,591 Valencia orange genes. The pathogenicity of<i> P. italicum </i>may be due to the activation of effectors, including 51 small secreted cysteine-rich proteins, 110 carbohydrate-active enzymes, and 12 G protein-coupled receptors. Additionally, 211 metabolites related to the interactions between<i> P. italicum </i>and Valencia orange were identified by gas chromatography-time of flight mass spectrography, three of which were further confirmed by ultra-high performance liquid chromatography triple quadrupole mass spectrometry. A metabolomics analysis indicated that <i>P. italicum </i>pathogenicity is associated with the sphingolipid and salicylic acid signaling pathways. Moreover, a correlation analysis between the metabolite contents and gene expression levels suggested that<i> P. italicum </i>induces carbohydrate metabolism in Valencia orange fruits as part of its infection strategy. This study provides useful information regarding the genomic determinants that drive the evolution of host specificity in<i> Penicillium </i>species and clarifies the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>. P. italicum GL_Gan1, a local strain in Guangzhou, China, was sequenced. Comparison of the genome of <i>P. italicum</i> GL_Gan1 with other pathogenic <i>Penicillium</i> species, <i>P. digitatum</i> and <i>P. expansum</i>, revealed that the expansion of protein families, genome restructuring, HGT, and positive selection pressure were related to the host range expansion of the analyzed <i>Penicillium</i> species. Moreover, gene gains or losses might be associated with the speciation of these <i>Penicillium</i> species. In addition, the molecular basis of host-plant specificity during the infection of Valencia orange (<i>Citrus sinensis</i>) by <i>P. italicum</i> was also elucidated by transcriptomic and metabolomics analysis. The data presented herein may be useful for further elucidating the molecular basis of the evolution of host specificity of <i>Penicillium</i> species and for illustrating the host-plant specificity during the infection of Valencia orange by <i>P. italicum</i>.