The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform

Shuang Bao Gun - One of the best experts on this subject based on the ideXlab platform.

  • EpigenetiC upregulation of ssC-miR-124a following treatment with Clostridium Perfringens beta2-toxin attenuates both apoptosis and inflammation in intestinal porCine epithelial Cells
    Archives of biochemistry and biophysics, 2021
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) is a globally reCognized zoonotiC pathogen. It has been reported that the beta2-toxin produCed by C. Perfringens Can Cause a variety of gastrointestinal diseases and even systemiC inflammation. MiCroRNA-124a (miR-124a) has been reported to play important roles in the host response to pathogeniC infeCtion. Although C. Perfringens beta2-toxin induCed injury in intestinal porCine epithelial (IPEC-J2) Cells has been established, the underlying moleCular meChanism is not Completely unraveled. Here we show that a signifiCant upregulation of ssC-miR-124a in IPEC-J2 Cells after beta2-toxin stimulation was assoCiated with the MiR-124A-1 and MiR-124A-2 gene promoter demethylation status. Importantly, overexpression of ssC-miR-124a signifiCantly inCreased Cell proliferation and deCreased apoptosis and CytotoxiCity in beta2-toxin treated IPEC-J2 Cells. TransfeCtion of IPEC-J2 Cells with ssC-miR-124a mimiC suppressed beta2-toxin induCed inflammation. On the Contrary, ssC-miR-124a inhibitor promoted aggravation of Cell apoptosis and exCessive damage. Furthermore, rho-assoCiated Coiled-Coil-Containing protein kinase 1 (ROCK1) was identified as the direCt target gene of ssC-miR-124a in IPEC-J2 Cells and its siRNA transfeCtion reversed the promotion of apoptosis and aggravation of Cellular damage induCed by ssC-miR-124a inhibitor. Overall, we speCulated that the miR-124A-1/2 gene was epigenetiCally regulated in IPEC-J2 Cells after beta2-toxin treatment. Upregulation of ssC-miR-124a may restrain ROCK1, and attenuate apoptosis and inflammation induCed by beta2-toxin that prevent IPEC-J2 Cells from severe damages. We disCover a new moleCular meChanism by whiCh IPEC-J2 Cells CounteraCt beta2-toxin‐induCed damage through the ssC-miR-124a/ROCK1 axis partially.

  • Inhibition of ssC-miCroRNA-140-5p ameliorates the Clostridium Perfringens beta2 toxin-induCed inflammatory response in IPEC-J2 Cells via the ERK1/2 and JNK pathways by targeting VEGFA.
    Molecular immunology, 2020
    Co-Authors: Ruirui Luo, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Xiaoli Gao, Wei Wang, Kaihui Xie, Shuang Bao Gun
    Abstract:

    Piglet diarrhea and even death due to Clostridium Perfringens (C. Perfringens) type C infeCtion have led to huge eConomiC losses in the pig industry worldwide. C. Perfringens beta2 (CPB2) toxin is the main virulenCe faCtor for this pathogen. MiR-140-5p Can exaCerbate toxin-induCed toxiCity of toxin to Cells by promoting oxidative stress. However, the role of pig miR-140-5p (ssC-miR-140-5p) in piglet diarrhea Caused by C. Perfringens type C has not been studied. Here, we study investigated the funCtion of ssC-miR-140-5p by generating an in vitro CPB2-induCed injury model in intestinal porCine epithelial (IPEC-J2) Cells. Our results revealed that transfeCtion with an ssC-miR-140-5p inhibitor signifiCantly inCreased the viability of CPB2-induCed IPEC-J2 Cells, deCrease the release of laCtate dehydrogenase (LDH) and reaCtive oxygen speCies (ROS), and inhibit inflammatory responses and apoptosis. In addition, vasCular endothelial growth faCtor A (VEGFA) was identified as a direCt target of ssC-miR-140-5p by luCiferase reporter assay. Western blot analysis showed that inhibition of ssC-miR-140-5p Could aCtivate the ERK1/2 signaling pathway and inhibit the JNK signaling pathway. In summary, we showed that down-regulation of ssC-miR-140-5p ameliorated CPB2-induCed inflammatory responses in IPEC-J2 Cells via the ERK1/2 and JNK signaling pathways by targeting VEGFA.

  • MiCroRNA-21-5p targets PDCD4 to modulate apoptosis and inflammatory response to Clostridium Perfringens beta2 toxin infeCtion in IPEC-J2 Cells.
    Developmental and comparative immunology, 2020
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    Clostridium Perfringens (C. Perfringens), a toxin-produCing enteriC pathogen, Causes a variety of intestinal infeCtions in humans and animals. C. Perfringens beta2 (CPB2) toxin has been Considered to be a strong virulenCe faCtor for C. Perfringens infeCtious enteriC diseases (CPED). Altered levels and funCtions of miCroRNA-21-5p (miR-21-5p) have been assoCiated with apoptosis and inflammation response in pathologiCal proCesses. However, little is known about its funCtional meChanism in CPED. Here, we found that miR-21-5p expressed in multiple tissues of pig, had a highest level in jejunum, and signifiCantly upregulated in intestinal porCine epithelial Cells (IPEC-J2) exposed to CPB2 toxin. Noteworthily, transfeCtion of CPB2-treated IPEC-J2 Cells with miR-21-5p mimiC inCreased Cell viability and BCl2 expression, as well as reduCed CytotoxiCity, apoptosis rates and Bax level. Moreover, overexpression of miR-21-5p signifiCantly suppressed the levels of interleukin (IL)-6, IL-8, TNF-α, IL-1β and nuClear faCtor-kappa B (NF-κB p65) aCtivity induCed by CPB2 toxin, whereas that of the IL-10 was inCreased in IPEC-J2 Cells. On the Contrary, transfeCtion of miR-21-5p inhibitor promoted CPB2-induCed Cell apoptosis and inflammation. Furthermore, we validated that programmed Cell death 4 (PDCD4) was strikingly downregulated in CPB2-treated IPEC-J2 Cells. PDCD4 exhibited opposing effeCts to those of miR-21-5p mimiC on IPEC-J2 Cells, and restoration of PDCD4 expression CounteraCted the suppressive effeCt of miR-21-5p on CPB2-induCed apoptosis and inflammatory response. ColleCtively, our findings demonstrated that miR-21-5p was involved in regulating the immune response triggered by CPB2 toxin and Contributed to proteCtive effeCts in CPB2-induCed CPED Cell model by targeting PDCD4.

  • Analyses of miRNA in the ileum of diarrheiC piglets Caused by Clostridium Perfringens type C.
    Microbial pathogenesis, 2019
    Co-Authors: Pengfei Wang, Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Qiao Li Yang, Ruirui Luo, Xiaoli Gao, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) type C is one of major pathogeniC Causing diarrhea and other intestinal inflammatory diseases in piglets, whiCh seriously affeCts the healthy development of the swine industries. Studies have found that miRNAs play important roles in regulating piglet diarrhea Challenged by pathogeniC E. Coli and Salmonella. However, little is known miRNAs in the ileum of diarrheiC piglets Caused by C. Perfringens type C. Therefore, we studied the expression profiles of the ileum miRNAs of 7-day-old piglets infeCted with C. Perfringens type C using small RNA-Seq, inCluding Control (IC), susCeptible (IS) and resistant (IR) groups. As a result, 53 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in ErbB signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway and Wnt signaling pathway. The expression Correlation analysis between miRNAs and target genes revealed that the expression of miR-7134-5p had negative Correlation with target NFATC4, miR-500 had negative Correlation with target ELK1, HSPA2 and IL7R, and miR-92b-3p had negative Correlation with target CLCF1 in ileum of IR vs IS group, suggesting that miR-7134-5p targeting to NFATC4, miR-500 targeting to ELK1, HSPA2 and IL7R, and miR-92b-3p targeting to CLCF1 were probably involved in piglet resisting C. Perfringens type C. The results will provide value resourCes for better understanding of the genetiC basis of C. Perfringens type C resistanCe in piglet and lays a new foundation for identifying novel markers of C. Perfringens type C resistanCe.

  • integrative analyses of long non Coding rna and mrna involved in piglet ileum immune response to Clostridium Perfringens type C infeCtion
    Frontiers in Cellular and Infection Microbiology, 2019
    Co-Authors: Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Hai Ren Shi, Qiao Li Yang, Pengfei Wang, Li Xia Liu, Sheng Guo Zhao, Shuang Bao Gun
    Abstract:

    Long non-Coding RNAs (lnCRNAs) have been shown to play important roles in regulating host immune and inflammatory responses to baCterial infeCtion. InfeCtion with Clostridium Perfringens (C. Perfringens), a food-borne zoonotiC pathogen, Can lead to a series of inflammatory diseases in human and piglet, greatly Challenging the healthy development of global pig industry. However, the roles of lnCRNAs involved in piglet immune response against C. Perfringens type C infeCtion remain unknown. In this study, the regulatory funCtions of ileum lnCRNAs and mRNAs were investigated in piglet immune response to C. Perfringens type C infeCtion among resistanCe (IR), susCeptibility (IS) and sham-inoCulation (Control, IC) groups. A total of 480 lnCRNAs and 3,669 mRNAs were signifiCantly differentially expressed, the differentially expressed lnCRNAs and mRNAs in the IR and IS groups were enriChed in various pathways of ABC transporters, olfaCtory transduCtion, PPAR signaling pathway, Chemokine signaling pathway and Toll-like reCeptor signaling pathway, involving in regulating piglet immune responses and resistanCe during infeCtion. There were 212 lnCRNAs and 505 target mRNAs found to have important assoCiation with C. Perfringens infeCtious diseases, furthermore, 25 dysregulated lnCRNAs Corresponding to 13 immune-related target mRNAs were identified to play potential roles in defense against baCterial infeCtion. In ConClusion, the results improve our understanding on the CharaCteristiCs of lnCRNAs and mRNAs on regulating host immune response against C. Perfringens type C infeCtion, whiCh will provide a referenCe for future researCh into exploring C. Perfringens-related diseases in human.

Xiao Yu Huang - One of the best experts on this subject based on the ideXlab platform.

  • EpigenetiC upregulation of ssC-miR-124a following treatment with Clostridium Perfringens beta2-toxin attenuates both apoptosis and inflammation in intestinal porCine epithelial Cells
    Archives of biochemistry and biophysics, 2021
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) is a globally reCognized zoonotiC pathogen. It has been reported that the beta2-toxin produCed by C. Perfringens Can Cause a variety of gastrointestinal diseases and even systemiC inflammation. MiCroRNA-124a (miR-124a) has been reported to play important roles in the host response to pathogeniC infeCtion. Although C. Perfringens beta2-toxin induCed injury in intestinal porCine epithelial (IPEC-J2) Cells has been established, the underlying moleCular meChanism is not Completely unraveled. Here we show that a signifiCant upregulation of ssC-miR-124a in IPEC-J2 Cells after beta2-toxin stimulation was assoCiated with the MiR-124A-1 and MiR-124A-2 gene promoter demethylation status. Importantly, overexpression of ssC-miR-124a signifiCantly inCreased Cell proliferation and deCreased apoptosis and CytotoxiCity in beta2-toxin treated IPEC-J2 Cells. TransfeCtion of IPEC-J2 Cells with ssC-miR-124a mimiC suppressed beta2-toxin induCed inflammation. On the Contrary, ssC-miR-124a inhibitor promoted aggravation of Cell apoptosis and exCessive damage. Furthermore, rho-assoCiated Coiled-Coil-Containing protein kinase 1 (ROCK1) was identified as the direCt target gene of ssC-miR-124a in IPEC-J2 Cells and its siRNA transfeCtion reversed the promotion of apoptosis and aggravation of Cellular damage induCed by ssC-miR-124a inhibitor. Overall, we speCulated that the miR-124A-1/2 gene was epigenetiCally regulated in IPEC-J2 Cells after beta2-toxin treatment. Upregulation of ssC-miR-124a may restrain ROCK1, and attenuate apoptosis and inflammation induCed by beta2-toxin that prevent IPEC-J2 Cells from severe damages. We disCover a new moleCular meChanism by whiCh IPEC-J2 Cells CounteraCt beta2-toxin‐induCed damage through the ssC-miR-124a/ROCK1 axis partially.

  • Inhibition of ssC-miCroRNA-140-5p ameliorates the Clostridium Perfringens beta2 toxin-induCed inflammatory response in IPEC-J2 Cells via the ERK1/2 and JNK pathways by targeting VEGFA.
    Molecular immunology, 2020
    Co-Authors: Ruirui Luo, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Xiaoli Gao, Wei Wang, Kaihui Xie, Shuang Bao Gun
    Abstract:

    Piglet diarrhea and even death due to Clostridium Perfringens (C. Perfringens) type C infeCtion have led to huge eConomiC losses in the pig industry worldwide. C. Perfringens beta2 (CPB2) toxin is the main virulenCe faCtor for this pathogen. MiR-140-5p Can exaCerbate toxin-induCed toxiCity of toxin to Cells by promoting oxidative stress. However, the role of pig miR-140-5p (ssC-miR-140-5p) in piglet diarrhea Caused by C. Perfringens type C has not been studied. Here, we study investigated the funCtion of ssC-miR-140-5p by generating an in vitro CPB2-induCed injury model in intestinal porCine epithelial (IPEC-J2) Cells. Our results revealed that transfeCtion with an ssC-miR-140-5p inhibitor signifiCantly inCreased the viability of CPB2-induCed IPEC-J2 Cells, deCrease the release of laCtate dehydrogenase (LDH) and reaCtive oxygen speCies (ROS), and inhibit inflammatory responses and apoptosis. In addition, vasCular endothelial growth faCtor A (VEGFA) was identified as a direCt target of ssC-miR-140-5p by luCiferase reporter assay. Western blot analysis showed that inhibition of ssC-miR-140-5p Could aCtivate the ERK1/2 signaling pathway and inhibit the JNK signaling pathway. In summary, we showed that down-regulation of ssC-miR-140-5p ameliorated CPB2-induCed inflammatory responses in IPEC-J2 Cells via the ERK1/2 and JNK signaling pathways by targeting VEGFA.

  • MiCroRNA-21-5p targets PDCD4 to modulate apoptosis and inflammatory response to Clostridium Perfringens beta2 toxin infeCtion in IPEC-J2 Cells.
    Developmental and comparative immunology, 2020
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    Clostridium Perfringens (C. Perfringens), a toxin-produCing enteriC pathogen, Causes a variety of intestinal infeCtions in humans and animals. C. Perfringens beta2 (CPB2) toxin has been Considered to be a strong virulenCe faCtor for C. Perfringens infeCtious enteriC diseases (CPED). Altered levels and funCtions of miCroRNA-21-5p (miR-21-5p) have been assoCiated with apoptosis and inflammation response in pathologiCal proCesses. However, little is known about its funCtional meChanism in CPED. Here, we found that miR-21-5p expressed in multiple tissues of pig, had a highest level in jejunum, and signifiCantly upregulated in intestinal porCine epithelial Cells (IPEC-J2) exposed to CPB2 toxin. Noteworthily, transfeCtion of CPB2-treated IPEC-J2 Cells with miR-21-5p mimiC inCreased Cell viability and BCl2 expression, as well as reduCed CytotoxiCity, apoptosis rates and Bax level. Moreover, overexpression of miR-21-5p signifiCantly suppressed the levels of interleukin (IL)-6, IL-8, TNF-α, IL-1β and nuClear faCtor-kappa B (NF-κB p65) aCtivity induCed by CPB2 toxin, whereas that of the IL-10 was inCreased in IPEC-J2 Cells. On the Contrary, transfeCtion of miR-21-5p inhibitor promoted CPB2-induCed Cell apoptosis and inflammation. Furthermore, we validated that programmed Cell death 4 (PDCD4) was strikingly downregulated in CPB2-treated IPEC-J2 Cells. PDCD4 exhibited opposing effeCts to those of miR-21-5p mimiC on IPEC-J2 Cells, and restoration of PDCD4 expression CounteraCted the suppressive effeCt of miR-21-5p on CPB2-induCed apoptosis and inflammatory response. ColleCtively, our findings demonstrated that miR-21-5p was involved in regulating the immune response triggered by CPB2 toxin and Contributed to proteCtive effeCts in CPB2-induCed CPED Cell model by targeting PDCD4.

  • Analyses of miRNA in the ileum of diarrheiC piglets Caused by Clostridium Perfringens type C.
    Microbial pathogenesis, 2019
    Co-Authors: Pengfei Wang, Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Qiao Li Yang, Ruirui Luo, Xiaoli Gao, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) type C is one of major pathogeniC Causing diarrhea and other intestinal inflammatory diseases in piglets, whiCh seriously affeCts the healthy development of the swine industries. Studies have found that miRNAs play important roles in regulating piglet diarrhea Challenged by pathogeniC E. Coli and Salmonella. However, little is known miRNAs in the ileum of diarrheiC piglets Caused by C. Perfringens type C. Therefore, we studied the expression profiles of the ileum miRNAs of 7-day-old piglets infeCted with C. Perfringens type C using small RNA-Seq, inCluding Control (IC), susCeptible (IS) and resistant (IR) groups. As a result, 53 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in ErbB signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway and Wnt signaling pathway. The expression Correlation analysis between miRNAs and target genes revealed that the expression of miR-7134-5p had negative Correlation with target NFATC4, miR-500 had negative Correlation with target ELK1, HSPA2 and IL7R, and miR-92b-3p had negative Correlation with target CLCF1 in ileum of IR vs IS group, suggesting that miR-7134-5p targeting to NFATC4, miR-500 targeting to ELK1, HSPA2 and IL7R, and miR-92b-3p targeting to CLCF1 were probably involved in piglet resisting C. Perfringens type C. The results will provide value resourCes for better understanding of the genetiC basis of C. Perfringens type C resistanCe in piglet and lays a new foundation for identifying novel markers of C. Perfringens type C resistanCe.

  • integrative analyses of long non Coding rna and mrna involved in piglet ileum immune response to Clostridium Perfringens type C infeCtion
    Frontiers in Cellular and Infection Microbiology, 2019
    Co-Authors: Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Hai Ren Shi, Qiao Li Yang, Pengfei Wang, Li Xia Liu, Sheng Guo Zhao, Shuang Bao Gun
    Abstract:

    Long non-Coding RNAs (lnCRNAs) have been shown to play important roles in regulating host immune and inflammatory responses to baCterial infeCtion. InfeCtion with Clostridium Perfringens (C. Perfringens), a food-borne zoonotiC pathogen, Can lead to a series of inflammatory diseases in human and piglet, greatly Challenging the healthy development of global pig industry. However, the roles of lnCRNAs involved in piglet immune response against C. Perfringens type C infeCtion remain unknown. In this study, the regulatory funCtions of ileum lnCRNAs and mRNAs were investigated in piglet immune response to C. Perfringens type C infeCtion among resistanCe (IR), susCeptibility (IS) and sham-inoCulation (Control, IC) groups. A total of 480 lnCRNAs and 3,669 mRNAs were signifiCantly differentially expressed, the differentially expressed lnCRNAs and mRNAs in the IR and IS groups were enriChed in various pathways of ABC transporters, olfaCtory transduCtion, PPAR signaling pathway, Chemokine signaling pathway and Toll-like reCeptor signaling pathway, involving in regulating piglet immune responses and resistanCe during infeCtion. There were 212 lnCRNAs and 505 target mRNAs found to have important assoCiation with C. Perfringens infeCtious diseases, furthermore, 25 dysregulated lnCRNAs Corresponding to 13 immune-related target mRNAs were identified to play potential roles in defense against baCterial infeCtion. In ConClusion, the results improve our understanding on the CharaCteristiCs of lnCRNAs and mRNAs on regulating host immune response against C. Perfringens type C infeCtion, whiCh will provide a referenCe for future researCh into exploring C. Perfringens-related diseases in human.

Zun Qiang Yan - One of the best experts on this subject based on the ideXlab platform.

  • EpigenetiC upregulation of ssC-miR-124a following treatment with Clostridium Perfringens beta2-toxin attenuates both apoptosis and inflammation in intestinal porCine epithelial Cells
    Archives of biochemistry and biophysics, 2021
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) is a globally reCognized zoonotiC pathogen. It has been reported that the beta2-toxin produCed by C. Perfringens Can Cause a variety of gastrointestinal diseases and even systemiC inflammation. MiCroRNA-124a (miR-124a) has been reported to play important roles in the host response to pathogeniC infeCtion. Although C. Perfringens beta2-toxin induCed injury in intestinal porCine epithelial (IPEC-J2) Cells has been established, the underlying moleCular meChanism is not Completely unraveled. Here we show that a signifiCant upregulation of ssC-miR-124a in IPEC-J2 Cells after beta2-toxin stimulation was assoCiated with the MiR-124A-1 and MiR-124A-2 gene promoter demethylation status. Importantly, overexpression of ssC-miR-124a signifiCantly inCreased Cell proliferation and deCreased apoptosis and CytotoxiCity in beta2-toxin treated IPEC-J2 Cells. TransfeCtion of IPEC-J2 Cells with ssC-miR-124a mimiC suppressed beta2-toxin induCed inflammation. On the Contrary, ssC-miR-124a inhibitor promoted aggravation of Cell apoptosis and exCessive damage. Furthermore, rho-assoCiated Coiled-Coil-Containing protein kinase 1 (ROCK1) was identified as the direCt target gene of ssC-miR-124a in IPEC-J2 Cells and its siRNA transfeCtion reversed the promotion of apoptosis and aggravation of Cellular damage induCed by ssC-miR-124a inhibitor. Overall, we speCulated that the miR-124A-1/2 gene was epigenetiCally regulated in IPEC-J2 Cells after beta2-toxin treatment. Upregulation of ssC-miR-124a may restrain ROCK1, and attenuate apoptosis and inflammation induCed by beta2-toxin that prevent IPEC-J2 Cells from severe damages. We disCover a new moleCular meChanism by whiCh IPEC-J2 Cells CounteraCt beta2-toxin‐induCed damage through the ssC-miR-124a/ROCK1 axis partially.

  • Inhibition of ssC-miCroRNA-140-5p ameliorates the Clostridium Perfringens beta2 toxin-induCed inflammatory response in IPEC-J2 Cells via the ERK1/2 and JNK pathways by targeting VEGFA.
    Molecular immunology, 2020
    Co-Authors: Ruirui Luo, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Xiaoli Gao, Wei Wang, Kaihui Xie, Shuang Bao Gun
    Abstract:

    Piglet diarrhea and even death due to Clostridium Perfringens (C. Perfringens) type C infeCtion have led to huge eConomiC losses in the pig industry worldwide. C. Perfringens beta2 (CPB2) toxin is the main virulenCe faCtor for this pathogen. MiR-140-5p Can exaCerbate toxin-induCed toxiCity of toxin to Cells by promoting oxidative stress. However, the role of pig miR-140-5p (ssC-miR-140-5p) in piglet diarrhea Caused by C. Perfringens type C has not been studied. Here, we study investigated the funCtion of ssC-miR-140-5p by generating an in vitro CPB2-induCed injury model in intestinal porCine epithelial (IPEC-J2) Cells. Our results revealed that transfeCtion with an ssC-miR-140-5p inhibitor signifiCantly inCreased the viability of CPB2-induCed IPEC-J2 Cells, deCrease the release of laCtate dehydrogenase (LDH) and reaCtive oxygen speCies (ROS), and inhibit inflammatory responses and apoptosis. In addition, vasCular endothelial growth faCtor A (VEGFA) was identified as a direCt target of ssC-miR-140-5p by luCiferase reporter assay. Western blot analysis showed that inhibition of ssC-miR-140-5p Could aCtivate the ERK1/2 signaling pathway and inhibit the JNK signaling pathway. In summary, we showed that down-regulation of ssC-miR-140-5p ameliorated CPB2-induCed inflammatory responses in IPEC-J2 Cells via the ERK1/2 and JNK signaling pathways by targeting VEGFA.

  • MiCroRNA-21-5p targets PDCD4 to modulate apoptosis and inflammatory response to Clostridium Perfringens beta2 toxin infeCtion in IPEC-J2 Cells.
    Developmental and comparative immunology, 2020
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    Clostridium Perfringens (C. Perfringens), a toxin-produCing enteriC pathogen, Causes a variety of intestinal infeCtions in humans and animals. C. Perfringens beta2 (CPB2) toxin has been Considered to be a strong virulenCe faCtor for C. Perfringens infeCtious enteriC diseases (CPED). Altered levels and funCtions of miCroRNA-21-5p (miR-21-5p) have been assoCiated with apoptosis and inflammation response in pathologiCal proCesses. However, little is known about its funCtional meChanism in CPED. Here, we found that miR-21-5p expressed in multiple tissues of pig, had a highest level in jejunum, and signifiCantly upregulated in intestinal porCine epithelial Cells (IPEC-J2) exposed to CPB2 toxin. Noteworthily, transfeCtion of CPB2-treated IPEC-J2 Cells with miR-21-5p mimiC inCreased Cell viability and BCl2 expression, as well as reduCed CytotoxiCity, apoptosis rates and Bax level. Moreover, overexpression of miR-21-5p signifiCantly suppressed the levels of interleukin (IL)-6, IL-8, TNF-α, IL-1β and nuClear faCtor-kappa B (NF-κB p65) aCtivity induCed by CPB2 toxin, whereas that of the IL-10 was inCreased in IPEC-J2 Cells. On the Contrary, transfeCtion of miR-21-5p inhibitor promoted CPB2-induCed Cell apoptosis and inflammation. Furthermore, we validated that programmed Cell death 4 (PDCD4) was strikingly downregulated in CPB2-treated IPEC-J2 Cells. PDCD4 exhibited opposing effeCts to those of miR-21-5p mimiC on IPEC-J2 Cells, and restoration of PDCD4 expression CounteraCted the suppressive effeCt of miR-21-5p on CPB2-induCed apoptosis and inflammatory response. ColleCtively, our findings demonstrated that miR-21-5p was involved in regulating the immune response triggered by CPB2 toxin and Contributed to proteCtive effeCts in CPB2-induCed CPED Cell model by targeting PDCD4.

  • Analyses of miRNA in the ileum of diarrheiC piglets Caused by Clostridium Perfringens type C.
    Microbial pathogenesis, 2019
    Co-Authors: Pengfei Wang, Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Qiao Li Yang, Ruirui Luo, Xiaoli Gao, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) type C is one of major pathogeniC Causing diarrhea and other intestinal inflammatory diseases in piglets, whiCh seriously affeCts the healthy development of the swine industries. Studies have found that miRNAs play important roles in regulating piglet diarrhea Challenged by pathogeniC E. Coli and Salmonella. However, little is known miRNAs in the ileum of diarrheiC piglets Caused by C. Perfringens type C. Therefore, we studied the expression profiles of the ileum miRNAs of 7-day-old piglets infeCted with C. Perfringens type C using small RNA-Seq, inCluding Control (IC), susCeptible (IS) and resistant (IR) groups. As a result, 53 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in ErbB signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway and Wnt signaling pathway. The expression Correlation analysis between miRNAs and target genes revealed that the expression of miR-7134-5p had negative Correlation with target NFATC4, miR-500 had negative Correlation with target ELK1, HSPA2 and IL7R, and miR-92b-3p had negative Correlation with target CLCF1 in ileum of IR vs IS group, suggesting that miR-7134-5p targeting to NFATC4, miR-500 targeting to ELK1, HSPA2 and IL7R, and miR-92b-3p targeting to CLCF1 were probably involved in piglet resisting C. Perfringens type C. The results will provide value resourCes for better understanding of the genetiC basis of C. Perfringens type C resistanCe in piglet and lays a new foundation for identifying novel markers of C. Perfringens type C resistanCe.

  • integrative analyses of long non Coding rna and mrna involved in piglet ileum immune response to Clostridium Perfringens type C infeCtion
    Frontiers in Cellular and Infection Microbiology, 2019
    Co-Authors: Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Hai Ren Shi, Qiao Li Yang, Pengfei Wang, Li Xia Liu, Sheng Guo Zhao, Shuang Bao Gun
    Abstract:

    Long non-Coding RNAs (lnCRNAs) have been shown to play important roles in regulating host immune and inflammatory responses to baCterial infeCtion. InfeCtion with Clostridium Perfringens (C. Perfringens), a food-borne zoonotiC pathogen, Can lead to a series of inflammatory diseases in human and piglet, greatly Challenging the healthy development of global pig industry. However, the roles of lnCRNAs involved in piglet immune response against C. Perfringens type C infeCtion remain unknown. In this study, the regulatory funCtions of ileum lnCRNAs and mRNAs were investigated in piglet immune response to C. Perfringens type C infeCtion among resistanCe (IR), susCeptibility (IS) and sham-inoCulation (Control, IC) groups. A total of 480 lnCRNAs and 3,669 mRNAs were signifiCantly differentially expressed, the differentially expressed lnCRNAs and mRNAs in the IR and IS groups were enriChed in various pathways of ABC transporters, olfaCtory transduCtion, PPAR signaling pathway, Chemokine signaling pathway and Toll-like reCeptor signaling pathway, involving in regulating piglet immune responses and resistanCe during infeCtion. There were 212 lnCRNAs and 505 target mRNAs found to have important assoCiation with C. Perfringens infeCtious diseases, furthermore, 25 dysregulated lnCRNAs Corresponding to 13 immune-related target mRNAs were identified to play potential roles in defense against baCterial infeCtion. In ConClusion, the results improve our understanding on the CharaCteristiCs of lnCRNAs and mRNAs on regulating host immune response against C. Perfringens type C infeCtion, whiCh will provide a referenCe for future researCh into exploring C. Perfringens-related diseases in human.

Pengfei Wang - One of the best experts on this subject based on the ideXlab platform.

  • EpigenetiC upregulation of ssC-miR-124a following treatment with Clostridium Perfringens beta2-toxin attenuates both apoptosis and inflammation in intestinal porCine epithelial Cells
    Archives of biochemistry and biophysics, 2021
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) is a globally reCognized zoonotiC pathogen. It has been reported that the beta2-toxin produCed by C. Perfringens Can Cause a variety of gastrointestinal diseases and even systemiC inflammation. MiCroRNA-124a (miR-124a) has been reported to play important roles in the host response to pathogeniC infeCtion. Although C. Perfringens beta2-toxin induCed injury in intestinal porCine epithelial (IPEC-J2) Cells has been established, the underlying moleCular meChanism is not Completely unraveled. Here we show that a signifiCant upregulation of ssC-miR-124a in IPEC-J2 Cells after beta2-toxin stimulation was assoCiated with the MiR-124A-1 and MiR-124A-2 gene promoter demethylation status. Importantly, overexpression of ssC-miR-124a signifiCantly inCreased Cell proliferation and deCreased apoptosis and CytotoxiCity in beta2-toxin treated IPEC-J2 Cells. TransfeCtion of IPEC-J2 Cells with ssC-miR-124a mimiC suppressed beta2-toxin induCed inflammation. On the Contrary, ssC-miR-124a inhibitor promoted aggravation of Cell apoptosis and exCessive damage. Furthermore, rho-assoCiated Coiled-Coil-Containing protein kinase 1 (ROCK1) was identified as the direCt target gene of ssC-miR-124a in IPEC-J2 Cells and its siRNA transfeCtion reversed the promotion of apoptosis and aggravation of Cellular damage induCed by ssC-miR-124a inhibitor. Overall, we speCulated that the miR-124A-1/2 gene was epigenetiCally regulated in IPEC-J2 Cells after beta2-toxin treatment. Upregulation of ssC-miR-124a may restrain ROCK1, and attenuate apoptosis and inflammation induCed by beta2-toxin that prevent IPEC-J2 Cells from severe damages. We disCover a new moleCular meChanism by whiCh IPEC-J2 Cells CounteraCt beta2-toxin‐induCed damage through the ssC-miR-124a/ROCK1 axis partially.

  • Inhibition of ssC-miCroRNA-140-5p ameliorates the Clostridium Perfringens beta2 toxin-induCed inflammatory response in IPEC-J2 Cells via the ERK1/2 and JNK pathways by targeting VEGFA.
    Molecular immunology, 2020
    Co-Authors: Ruirui Luo, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Xiaoli Gao, Wei Wang, Kaihui Xie, Shuang Bao Gun
    Abstract:

    Piglet diarrhea and even death due to Clostridium Perfringens (C. Perfringens) type C infeCtion have led to huge eConomiC losses in the pig industry worldwide. C. Perfringens beta2 (CPB2) toxin is the main virulenCe faCtor for this pathogen. MiR-140-5p Can exaCerbate toxin-induCed toxiCity of toxin to Cells by promoting oxidative stress. However, the role of pig miR-140-5p (ssC-miR-140-5p) in piglet diarrhea Caused by C. Perfringens type C has not been studied. Here, we study investigated the funCtion of ssC-miR-140-5p by generating an in vitro CPB2-induCed injury model in intestinal porCine epithelial (IPEC-J2) Cells. Our results revealed that transfeCtion with an ssC-miR-140-5p inhibitor signifiCantly inCreased the viability of CPB2-induCed IPEC-J2 Cells, deCrease the release of laCtate dehydrogenase (LDH) and reaCtive oxygen speCies (ROS), and inhibit inflammatory responses and apoptosis. In addition, vasCular endothelial growth faCtor A (VEGFA) was identified as a direCt target of ssC-miR-140-5p by luCiferase reporter assay. Western blot analysis showed that inhibition of ssC-miR-140-5p Could aCtivate the ERK1/2 signaling pathway and inhibit the JNK signaling pathway. In summary, we showed that down-regulation of ssC-miR-140-5p ameliorated CPB2-induCed inflammatory responses in IPEC-J2 Cells via the ERK1/2 and JNK signaling pathways by targeting VEGFA.

  • MiCroRNA-21-5p targets PDCD4 to modulate apoptosis and inflammatory response to Clostridium Perfringens beta2 toxin infeCtion in IPEC-J2 Cells.
    Developmental and comparative immunology, 2020
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    Clostridium Perfringens (C. Perfringens), a toxin-produCing enteriC pathogen, Causes a variety of intestinal infeCtions in humans and animals. C. Perfringens beta2 (CPB2) toxin has been Considered to be a strong virulenCe faCtor for C. Perfringens infeCtious enteriC diseases (CPED). Altered levels and funCtions of miCroRNA-21-5p (miR-21-5p) have been assoCiated with apoptosis and inflammation response in pathologiCal proCesses. However, little is known about its funCtional meChanism in CPED. Here, we found that miR-21-5p expressed in multiple tissues of pig, had a highest level in jejunum, and signifiCantly upregulated in intestinal porCine epithelial Cells (IPEC-J2) exposed to CPB2 toxin. Noteworthily, transfeCtion of CPB2-treated IPEC-J2 Cells with miR-21-5p mimiC inCreased Cell viability and BCl2 expression, as well as reduCed CytotoxiCity, apoptosis rates and Bax level. Moreover, overexpression of miR-21-5p signifiCantly suppressed the levels of interleukin (IL)-6, IL-8, TNF-α, IL-1β and nuClear faCtor-kappa B (NF-κB p65) aCtivity induCed by CPB2 toxin, whereas that of the IL-10 was inCreased in IPEC-J2 Cells. On the Contrary, transfeCtion of miR-21-5p inhibitor promoted CPB2-induCed Cell apoptosis and inflammation. Furthermore, we validated that programmed Cell death 4 (PDCD4) was strikingly downregulated in CPB2-treated IPEC-J2 Cells. PDCD4 exhibited opposing effeCts to those of miR-21-5p mimiC on IPEC-J2 Cells, and restoration of PDCD4 expression CounteraCted the suppressive effeCt of miR-21-5p on CPB2-induCed apoptosis and inflammatory response. ColleCtively, our findings demonstrated that miR-21-5p was involved in regulating the immune response triggered by CPB2 toxin and Contributed to proteCtive effeCts in CPB2-induCed CPED Cell model by targeting PDCD4.

  • Analyses of miRNA in the ileum of diarrheiC piglets Caused by Clostridium Perfringens type C.
    Microbial pathogenesis, 2019
    Co-Authors: Pengfei Wang, Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Qiao Li Yang, Ruirui Luo, Xiaoli Gao, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) type C is one of major pathogeniC Causing diarrhea and other intestinal inflammatory diseases in piglets, whiCh seriously affeCts the healthy development of the swine industries. Studies have found that miRNAs play important roles in regulating piglet diarrhea Challenged by pathogeniC E. Coli and Salmonella. However, little is known miRNAs in the ileum of diarrheiC piglets Caused by C. Perfringens type C. Therefore, we studied the expression profiles of the ileum miRNAs of 7-day-old piglets infeCted with C. Perfringens type C using small RNA-Seq, inCluding Control (IC), susCeptible (IS) and resistant (IR) groups. As a result, 53 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in ErbB signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway and Wnt signaling pathway. The expression Correlation analysis between miRNAs and target genes revealed that the expression of miR-7134-5p had negative Correlation with target NFATC4, miR-500 had negative Correlation with target ELK1, HSPA2 and IL7R, and miR-92b-3p had negative Correlation with target CLCF1 in ileum of IR vs IS group, suggesting that miR-7134-5p targeting to NFATC4, miR-500 targeting to ELK1, HSPA2 and IL7R, and miR-92b-3p targeting to CLCF1 were probably involved in piglet resisting C. Perfringens type C. The results will provide value resourCes for better understanding of the genetiC basis of C. Perfringens type C resistanCe in piglet and lays a new foundation for identifying novel markers of C. Perfringens type C resistanCe.

  • integrative analyses of long non Coding rna and mrna involved in piglet ileum immune response to Clostridium Perfringens type C infeCtion
    Frontiers in Cellular and Infection Microbiology, 2019
    Co-Authors: Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Hai Ren Shi, Qiao Li Yang, Pengfei Wang, Li Xia Liu, Sheng Guo Zhao, Shuang Bao Gun
    Abstract:

    Long non-Coding RNAs (lnCRNAs) have been shown to play important roles in regulating host immune and inflammatory responses to baCterial infeCtion. InfeCtion with Clostridium Perfringens (C. Perfringens), a food-borne zoonotiC pathogen, Can lead to a series of inflammatory diseases in human and piglet, greatly Challenging the healthy development of global pig industry. However, the roles of lnCRNAs involved in piglet immune response against C. Perfringens type C infeCtion remain unknown. In this study, the regulatory funCtions of ileum lnCRNAs and mRNAs were investigated in piglet immune response to C. Perfringens type C infeCtion among resistanCe (IR), susCeptibility (IS) and sham-inoCulation (Control, IC) groups. A total of 480 lnCRNAs and 3,669 mRNAs were signifiCantly differentially expressed, the differentially expressed lnCRNAs and mRNAs in the IR and IS groups were enriChed in various pathways of ABC transporters, olfaCtory transduCtion, PPAR signaling pathway, Chemokine signaling pathway and Toll-like reCeptor signaling pathway, involving in regulating piglet immune responses and resistanCe during infeCtion. There were 212 lnCRNAs and 505 target mRNAs found to have important assoCiation with C. Perfringens infeCtious diseases, furthermore, 25 dysregulated lnCRNAs Corresponding to 13 immune-related target mRNAs were identified to play potential roles in defense against baCterial infeCtion. In ConClusion, the results improve our understanding on the CharaCteristiCs of lnCRNAs and mRNAs on regulating host immune response against C. Perfringens type C infeCtion, whiCh will provide a referenCe for future researCh into exploring C. Perfringens-related diseases in human.

Qiao Li Yang - One of the best experts on this subject based on the ideXlab platform.

  • EpigenetiC upregulation of ssC-miR-124a following treatment with Clostridium Perfringens beta2-toxin attenuates both apoptosis and inflammation in intestinal porCine epithelial Cells
    Archives of biochemistry and biophysics, 2021
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) is a globally reCognized zoonotiC pathogen. It has been reported that the beta2-toxin produCed by C. Perfringens Can Cause a variety of gastrointestinal diseases and even systemiC inflammation. MiCroRNA-124a (miR-124a) has been reported to play important roles in the host response to pathogeniC infeCtion. Although C. Perfringens beta2-toxin induCed injury in intestinal porCine epithelial (IPEC-J2) Cells has been established, the underlying moleCular meChanism is not Completely unraveled. Here we show that a signifiCant upregulation of ssC-miR-124a in IPEC-J2 Cells after beta2-toxin stimulation was assoCiated with the MiR-124A-1 and MiR-124A-2 gene promoter demethylation status. Importantly, overexpression of ssC-miR-124a signifiCantly inCreased Cell proliferation and deCreased apoptosis and CytotoxiCity in beta2-toxin treated IPEC-J2 Cells. TransfeCtion of IPEC-J2 Cells with ssC-miR-124a mimiC suppressed beta2-toxin induCed inflammation. On the Contrary, ssC-miR-124a inhibitor promoted aggravation of Cell apoptosis and exCessive damage. Furthermore, rho-assoCiated Coiled-Coil-Containing protein kinase 1 (ROCK1) was identified as the direCt target gene of ssC-miR-124a in IPEC-J2 Cells and its siRNA transfeCtion reversed the promotion of apoptosis and aggravation of Cellular damage induCed by ssC-miR-124a inhibitor. Overall, we speCulated that the miR-124A-1/2 gene was epigenetiCally regulated in IPEC-J2 Cells after beta2-toxin treatment. Upregulation of ssC-miR-124a may restrain ROCK1, and attenuate apoptosis and inflammation induCed by beta2-toxin that prevent IPEC-J2 Cells from severe damages. We disCover a new moleCular meChanism by whiCh IPEC-J2 Cells CounteraCt beta2-toxin‐induCed damage through the ssC-miR-124a/ROCK1 axis partially.

  • Inhibition of ssC-miCroRNA-140-5p ameliorates the Clostridium Perfringens beta2 toxin-induCed inflammatory response in IPEC-J2 Cells via the ERK1/2 and JNK pathways by targeting VEGFA.
    Molecular immunology, 2020
    Co-Authors: Ruirui Luo, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Xiaoli Gao, Wei Wang, Kaihui Xie, Shuang Bao Gun
    Abstract:

    Piglet diarrhea and even death due to Clostridium Perfringens (C. Perfringens) type C infeCtion have led to huge eConomiC losses in the pig industry worldwide. C. Perfringens beta2 (CPB2) toxin is the main virulenCe faCtor for this pathogen. MiR-140-5p Can exaCerbate toxin-induCed toxiCity of toxin to Cells by promoting oxidative stress. However, the role of pig miR-140-5p (ssC-miR-140-5p) in piglet diarrhea Caused by C. Perfringens type C has not been studied. Here, we study investigated the funCtion of ssC-miR-140-5p by generating an in vitro CPB2-induCed injury model in intestinal porCine epithelial (IPEC-J2) Cells. Our results revealed that transfeCtion with an ssC-miR-140-5p inhibitor signifiCantly inCreased the viability of CPB2-induCed IPEC-J2 Cells, deCrease the release of laCtate dehydrogenase (LDH) and reaCtive oxygen speCies (ROS), and inhibit inflammatory responses and apoptosis. In addition, vasCular endothelial growth faCtor A (VEGFA) was identified as a direCt target of ssC-miR-140-5p by luCiferase reporter assay. Western blot analysis showed that inhibition of ssC-miR-140-5p Could aCtivate the ERK1/2 signaling pathway and inhibit the JNK signaling pathway. In summary, we showed that down-regulation of ssC-miR-140-5p ameliorated CPB2-induCed inflammatory responses in IPEC-J2 Cells via the ERK1/2 and JNK signaling pathways by targeting VEGFA.

  • MiCroRNA-21-5p targets PDCD4 to modulate apoptosis and inflammatory response to Clostridium Perfringens beta2 toxin infeCtion in IPEC-J2 Cells.
    Developmental and comparative immunology, 2020
    Co-Authors: Xiaoli Gao, Xiao Yu Huang, Zun Qiang Yan, Qiao Li Yang, Pengfei Wang, Ruirui Luo, Wei Wang, Kaihui Xie, Shengwei Zhang, Shuang Bao Gun
    Abstract:

    Clostridium Perfringens (C. Perfringens), a toxin-produCing enteriC pathogen, Causes a variety of intestinal infeCtions in humans and animals. C. Perfringens beta2 (CPB2) toxin has been Considered to be a strong virulenCe faCtor for C. Perfringens infeCtious enteriC diseases (CPED). Altered levels and funCtions of miCroRNA-21-5p (miR-21-5p) have been assoCiated with apoptosis and inflammation response in pathologiCal proCesses. However, little is known about its funCtional meChanism in CPED. Here, we found that miR-21-5p expressed in multiple tissues of pig, had a highest level in jejunum, and signifiCantly upregulated in intestinal porCine epithelial Cells (IPEC-J2) exposed to CPB2 toxin. Noteworthily, transfeCtion of CPB2-treated IPEC-J2 Cells with miR-21-5p mimiC inCreased Cell viability and BCl2 expression, as well as reduCed CytotoxiCity, apoptosis rates and Bax level. Moreover, overexpression of miR-21-5p signifiCantly suppressed the levels of interleukin (IL)-6, IL-8, TNF-α, IL-1β and nuClear faCtor-kappa B (NF-κB p65) aCtivity induCed by CPB2 toxin, whereas that of the IL-10 was inCreased in IPEC-J2 Cells. On the Contrary, transfeCtion of miR-21-5p inhibitor promoted CPB2-induCed Cell apoptosis and inflammation. Furthermore, we validated that programmed Cell death 4 (PDCD4) was strikingly downregulated in CPB2-treated IPEC-J2 Cells. PDCD4 exhibited opposing effeCts to those of miR-21-5p mimiC on IPEC-J2 Cells, and restoration of PDCD4 expression CounteraCted the suppressive effeCt of miR-21-5p on CPB2-induCed apoptosis and inflammatory response. ColleCtively, our findings demonstrated that miR-21-5p was involved in regulating the immune response triggered by CPB2 toxin and Contributed to proteCtive effeCts in CPB2-induCed CPED Cell model by targeting PDCD4.

  • Analyses of miRNA in the ileum of diarrheiC piglets Caused by Clostridium Perfringens type C.
    Microbial pathogenesis, 2019
    Co-Authors: Pengfei Wang, Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Qiao Li Yang, Ruirui Luo, Xiaoli Gao, Shuang Bao Gun
    Abstract:

    AbstraCt Clostridium Perfringens (C. Perfringens) type C is one of major pathogeniC Causing diarrhea and other intestinal inflammatory diseases in piglets, whiCh seriously affeCts the healthy development of the swine industries. Studies have found that miRNAs play important roles in regulating piglet diarrhea Challenged by pathogeniC E. Coli and Salmonella. However, little is known miRNAs in the ileum of diarrheiC piglets Caused by C. Perfringens type C. Therefore, we studied the expression profiles of the ileum miRNAs of 7-day-old piglets infeCted with C. Perfringens type C using small RNA-Seq, inCluding Control (IC), susCeptible (IS) and resistant (IR) groups. As a result, 53 differentially expressed miRNAs were found. KEGG pathway analysis for target genes revealed that these miRNAs were involved in ErbB signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway and Wnt signaling pathway. The expression Correlation analysis between miRNAs and target genes revealed that the expression of miR-7134-5p had negative Correlation with target NFATC4, miR-500 had negative Correlation with target ELK1, HSPA2 and IL7R, and miR-92b-3p had negative Correlation with target CLCF1 in ileum of IR vs IS group, suggesting that miR-7134-5p targeting to NFATC4, miR-500 targeting to ELK1, HSPA2 and IL7R, and miR-92b-3p targeting to CLCF1 were probably involved in piglet resisting C. Perfringens type C. The results will provide value resourCes for better understanding of the genetiC basis of C. Perfringens type C resistanCe in piglet and lays a new foundation for identifying novel markers of C. Perfringens type C resistanCe.

  • integrative analyses of long non Coding rna and mrna involved in piglet ileum immune response to Clostridium Perfringens type C infeCtion
    Frontiers in Cellular and Infection Microbiology, 2019
    Co-Authors: Xiao Yu Huang, Wen Yang Sun, Zun Qiang Yan, Hai Ren Shi, Qiao Li Yang, Pengfei Wang, Li Xia Liu, Sheng Guo Zhao, Shuang Bao Gun
    Abstract:

    Long non-Coding RNAs (lnCRNAs) have been shown to play important roles in regulating host immune and inflammatory responses to baCterial infeCtion. InfeCtion with Clostridium Perfringens (C. Perfringens), a food-borne zoonotiC pathogen, Can lead to a series of inflammatory diseases in human and piglet, greatly Challenging the healthy development of global pig industry. However, the roles of lnCRNAs involved in piglet immune response against C. Perfringens type C infeCtion remain unknown. In this study, the regulatory funCtions of ileum lnCRNAs and mRNAs were investigated in piglet immune response to C. Perfringens type C infeCtion among resistanCe (IR), susCeptibility (IS) and sham-inoCulation (Control, IC) groups. A total of 480 lnCRNAs and 3,669 mRNAs were signifiCantly differentially expressed, the differentially expressed lnCRNAs and mRNAs in the IR and IS groups were enriChed in various pathways of ABC transporters, olfaCtory transduCtion, PPAR signaling pathway, Chemokine signaling pathway and Toll-like reCeptor signaling pathway, involving in regulating piglet immune responses and resistanCe during infeCtion. There were 212 lnCRNAs and 505 target mRNAs found to have important assoCiation with C. Perfringens infeCtious diseases, furthermore, 25 dysregulated lnCRNAs Corresponding to 13 immune-related target mRNAs were identified to play potential roles in defense against baCterial infeCtion. In ConClusion, the results improve our understanding on the CharaCteristiCs of lnCRNAs and mRNAs on regulating host immune response against C. Perfringens type C infeCtion, whiCh will provide a referenCe for future researCh into exploring C. Perfringens-related diseases in human.