The Experts below are selected from a list of 30717 Experts worldwide ranked by ideXlab platform

Francisco P Chavez - One of the best experts on this subject based on the ideXlab platform.

  • in vivo Host Pathogen Interaction as revealed by global proteomic profiling of zebrafish larvae
    Frontiers in Cellular and Infection Microbiology, 2017
    Co-Authors: Francisco Diazpascual, Javiera Ortizseverin, Macarena A Varas, Miguel L Allende, Francisco P Chavez
    Abstract:

    The outcome of a Host-Pathogen Interaction is determined by the conditions of the Host, the Pathogen, and the environment. Although numerous proteomic studies of in vitro-grown microbial Pathogens have been performed, in vivo proteomic approaches are still rare. In addition, increasing evidence supports that in vitro studies inadequately reflect in vivo conditions. Choosing the proper Host is essential to detect the expression of proteins from the Pathogen in vivo. Numerous studies have demonstrated the suitability of zebrafish (Danio rerio) embryos as a model to in vivo studies of Pseudomonas aeruginosa infection. In most zebrafish-Pathogen studies, infection is achieved by microinjection of bacteria into the larvae. However, few reports using static immersion of bacterial Pathogens have been published. In this study we infected 3 days post-fertilization (DPF) zebrafish larvae with P. aeruginosa PAO1 by immersion and injection and tracked the in vivo immune response by the zebrafish. Additionally, by using non-isotopic (Q-exactive) metaproteomics we simultaneously evaluated the proteomic response of the Pathogen (P. aeruginosa PAO1) and the Host (zebrafish). We found some zebrafish metabolic pathways, such as hypoxia response via HIF activation pathway, were exclusively enriched in the larvae exposed by static immersion. In contrast, we found that inflammation mediated by chemokine and cytokine signaling pathways was exclusively enriched in the larvae exposed by injection, while the integrin signaling pathway and angiogenesis were solely enriched in the larvae exposed by immersion. We also found important virulence factors from P. aeruginosa that were enriched only after exposure by injection, such as the Type-III secretion system and flagella-associated proteins. On the other hand, P. aeruginosa proteins involved in processes like biofilm formation, and cellular responses to antibiotic and starvation were enriched exclusively after exposure by immersion. We demonstrated the suitability of zebrafish embryos as a model for in vivo Host-Pathogen based proteomic studies in P. aeruginosa. Our global proteomic profiling identifies novel molecular signatures that give systematic insight into zebrafish-Pseudomonas Interaction.

  • in vivo Host Pathogen Interaction as revealed by global proteomic profiling of zebrafish larvae
    bioRxiv, 2017
    Co-Authors: Francisco Diazpascual, Javiera Ortizseverin, Macarena A Varas, Miguel L Allende, Francisco P Chavez
    Abstract:

    The outcome of a Host-Pathogen Interaction is determined by the conditions of the Host, the Pathogen, and the environment. Although numerous proteomic studies of in vitro-grown microbial Pathogens have been performed, in vivo proteomic approaches are still rare. In addition, increasing evidence supports that in vitro studies inadequately reflect in vivo conditions. Choosing the proper Host is essential to detect the expression of proteins from the Pathogen in vivo. Numerous studies have demonstrated the suitability of zebrafish (Danio rerio) embryos as a model to in vivo studies of Pseudomonas aeruginosa infection. In most zebrafish-Pathogen studies, infection is achieved by microinjection of bacteria into the larvae. However, few reports using static immersion of bacterial Pathogens have been published. In this study we infected 3 days post-fertilization (DPF) zebrafish larvae with P. aeruginosa PAO1 by immersion and injection and tracked the in vivo immune response by the zebrafish. Additionally, by using non-isotopic (Q-exactive) metaproteomics we simultaneously evaluated the proteomic response of the Pathogen (P. aeruginosa PAO1) and the Host (zebrafish). We found some zebrafish metabolic pathways, such as hypoxia response via HIF activation pathway, exclusively enriched in the larvae exposed by static immersion. In contrast, we found that inflammation mediated by chemokine and cytokine signaling pathways was exclusively enriched in the larvae exposed by injection, while the integrin signaling pathway and angiogenesis were solely enriched in the larvae exposed by immersion. We also found important virulence factors from P. aeruginosa that were enriched only after exposure by injection, such as the Type-III secretion system and flagella-associated proteins. On the other hand, P. aeruginosa proteins involved in processes like biofilm formation, cellular responses to antibiotic and starvation were enriched exclusively after an exposure by immersion. We demonstrated the suitability of zebrafish embryos as a model for in vivo Host-Pathogen based proteomic studies in P. aeruginosa. Our global proteomic profiling identifies novel molecular signatures that give systematic insight into zebrafish-Pseudomonas Interaction.

Catharina Svanborg - One of the best experts on this subject based on the ideXlab platform.

  • Susceptibility to acute pyelonephritis or asymptomatic bacteriuria: Host–Pathogen Interaction in urinary tract infections
    Pediatric Nephrology, 2012
    Co-Authors: Bryndis Ragnarsdottir, Catharina Svanborg
    Abstract:

    Our knowledge of the molecular mechanisms of urinary tract infection (UTI) Pathogenesis has advanced greatly in recent years. In this review, we provide a general background of UTI Pathogenesis, followed by an update on the mechanisms of UTI susceptibility, with a particular focus on genetic variation affecting innate immunity. The innate immune response of the Host is critically important in the antibacterial defence mechanisms of the urinary tract, and bacterial clearance normally proceeds without sequelae. However, slight dysfunctions in these mechanisms may result in acute disease and tissue destruction. The symptoms of acute pyelonephritis are caused by the innate immune response, and inflammation in the urinary tract decreases renal tubular function and may give rise to renal scarring, especially in paediatric patients. In contrast, in children with asymptomatic bacteriuria (ABU), bacteria persist without causing symptoms or pathology. Pathogenic agents trigger a response determined by their virulence factors, mediating adherence to the urinary tract mucosa, signalling through Toll-like receptors (TLRs) and activating the defence mechanisms. In ABU strains, such virulence factors are mostly not expressed. However, the influence of the Host on UTI severity cannot be overestimated, and rapid progress is being made in clarifying Host susceptibility mechanisms. For example, genetic alterations that reduce TLR4 function are associated with ABU, while polymorphisms reducing IRF3 or CXCR1 expression are associated with acute pyelonephritis and an increased risk for renal scarring. It should be plausible to “individualize” diagnosis and therapy by combining information on bacterial virulence and the Host response.

  • susceptibility to acute pyelonephritis or asymptomatic bacteriuria Host Pathogen Interaction in urinary tract infections
    Pediatric Nephrology, 2012
    Co-Authors: Bryndis Ragnarsdottir, Catharina Svanborg
    Abstract:

    Our knowledge of the molecular mechanisms of urinary tract infection (UTI) Pathogenesis has advanced greatly in recent years. In this review, we provide a general background of UTI Pathogenesis, followed by an update on the mechanisms of UTI susceptibility, with a particular focus on genetic variation affecting innate immunity. The innate immune response of the Host is critically important in the antibacterial defence mechanisms of the urinary tract, and bacterial clearance normally proceeds without sequelae. However, slight dysfunctions in these mechanisms may result in acute disease and tissue destruction. The symptoms of acute pyelonephritis are caused by the innate immune response, and inflammation in the urinary tract decreases renal tubular function and may give rise to renal scarring, especially in paediatric patients. In contrast, in children with asymptomatic bacteriuria (ABU), bacteria persist without causing symptoms or pathology. Pathogenic agents trigger a response determined by their virulence factors, mediating adherence to the urinary tract mucosa, signalling through Toll-like receptors (TLRs) and activating the defence mechanisms. In ABU strains, such virulence factors are mostly not expressed. However, the influence of the Host on UTI severity cannot be overestimated, and rapid progress is being made in clarifying Host susceptibility mechanisms. For example, genetic alterations that reduce TLR4 function are associated with ABU, while polymorphisms reducing IRF3 or CXCR1 expression are associated with acute pyelonephritis and an increased risk for renal scarring. It should be plausible to “individualize” diagnosis and therapy by combining information on bacterial virulence and the Host response.

Roland Brosch - One of the best experts on this subject based on the ideXlab platform.

  • ESX/type VII secretion systems and their role in Host–Pathogen Interaction
    Current Opinion in Microbiology, 2009
    Co-Authors: Roxane Simeone, Daria Bottai, Roland Brosch
    Abstract:

    The ESX-1 system is responsible for the secretion of the prototypic ESX proteins, namely the 6 kDa early secreted antigenic target (ESAT-6) and the 10 kDa culture filtrate protein (CFP-10). These two proteins, which form a 1:1 heterodimeric complex, are among the most important proteins of Mycobacterium tuberculosis involved in Host-Pathogen Interaction. They induce a strong T cell mediated immune response, are apparently involved in membrane and/or Host-cell lysis and represent key virulence factors. There are four other paralogous ESX systems in M. tuberculosis, some of which are essential for in vitro growth. ESX systems also exist in many other actinobacteria and Gram-positive bacteria, and have recently been suggested to be named type VII secretion systems.

  • esx type vii secretion systems and their role in Host Pathogen Interaction
    Current Opinion in Microbiology, 2009
    Co-Authors: Roxane Simeone, Daria Bottai, Roland Brosch
    Abstract:

    The ESX-1 system is responsible for the secretion of the prototypic ESX proteins, namely the 6 kDa early secreted antigenic target (ESAT-6) and the 10 kDa culture filtrate protein (CFP-10). These two proteins, which form a 1:1 heterodimeric complex, are among the most important proteins of Mycobacterium tuberculosis involved in Host-Pathogen Interaction. They induce a strong T cell mediated immune response, are apparently involved in membrane and/or Host-cell lysis and represent key virulence factors. There are four other paralogous ESX systems in M. tuberculosis, some of which are essential for in vitro growth. ESX systems also exist in many other actinobacteria and Gram-positive bacteria, and have recently been suggested to be named type VII secretion systems.

Francisco Diazpascual - One of the best experts on this subject based on the ideXlab platform.

  • in vivo Host Pathogen Interaction as revealed by global proteomic profiling of zebrafish larvae
    Frontiers in Cellular and Infection Microbiology, 2017
    Co-Authors: Francisco Diazpascual, Javiera Ortizseverin, Macarena A Varas, Miguel L Allende, Francisco P Chavez
    Abstract:

    The outcome of a Host-Pathogen Interaction is determined by the conditions of the Host, the Pathogen, and the environment. Although numerous proteomic studies of in vitro-grown microbial Pathogens have been performed, in vivo proteomic approaches are still rare. In addition, increasing evidence supports that in vitro studies inadequately reflect in vivo conditions. Choosing the proper Host is essential to detect the expression of proteins from the Pathogen in vivo. Numerous studies have demonstrated the suitability of zebrafish (Danio rerio) embryos as a model to in vivo studies of Pseudomonas aeruginosa infection. In most zebrafish-Pathogen studies, infection is achieved by microinjection of bacteria into the larvae. However, few reports using static immersion of bacterial Pathogens have been published. In this study we infected 3 days post-fertilization (DPF) zebrafish larvae with P. aeruginosa PAO1 by immersion and injection and tracked the in vivo immune response by the zebrafish. Additionally, by using non-isotopic (Q-exactive) metaproteomics we simultaneously evaluated the proteomic response of the Pathogen (P. aeruginosa PAO1) and the Host (zebrafish). We found some zebrafish metabolic pathways, such as hypoxia response via HIF activation pathway, were exclusively enriched in the larvae exposed by static immersion. In contrast, we found that inflammation mediated by chemokine and cytokine signaling pathways was exclusively enriched in the larvae exposed by injection, while the integrin signaling pathway and angiogenesis were solely enriched in the larvae exposed by immersion. We also found important virulence factors from P. aeruginosa that were enriched only after exposure by injection, such as the Type-III secretion system and flagella-associated proteins. On the other hand, P. aeruginosa proteins involved in processes like biofilm formation, and cellular responses to antibiotic and starvation were enriched exclusively after exposure by immersion. We demonstrated the suitability of zebrafish embryos as a model for in vivo Host-Pathogen based proteomic studies in P. aeruginosa. Our global proteomic profiling identifies novel molecular signatures that give systematic insight into zebrafish-Pseudomonas Interaction.

  • in vivo Host Pathogen Interaction as revealed by global proteomic profiling of zebrafish larvae
    bioRxiv, 2017
    Co-Authors: Francisco Diazpascual, Javiera Ortizseverin, Macarena A Varas, Miguel L Allende, Francisco P Chavez
    Abstract:

    The outcome of a Host-Pathogen Interaction is determined by the conditions of the Host, the Pathogen, and the environment. Although numerous proteomic studies of in vitro-grown microbial Pathogens have been performed, in vivo proteomic approaches are still rare. In addition, increasing evidence supports that in vitro studies inadequately reflect in vivo conditions. Choosing the proper Host is essential to detect the expression of proteins from the Pathogen in vivo. Numerous studies have demonstrated the suitability of zebrafish (Danio rerio) embryos as a model to in vivo studies of Pseudomonas aeruginosa infection. In most zebrafish-Pathogen studies, infection is achieved by microinjection of bacteria into the larvae. However, few reports using static immersion of bacterial Pathogens have been published. In this study we infected 3 days post-fertilization (DPF) zebrafish larvae with P. aeruginosa PAO1 by immersion and injection and tracked the in vivo immune response by the zebrafish. Additionally, by using non-isotopic (Q-exactive) metaproteomics we simultaneously evaluated the proteomic response of the Pathogen (P. aeruginosa PAO1) and the Host (zebrafish). We found some zebrafish metabolic pathways, such as hypoxia response via HIF activation pathway, exclusively enriched in the larvae exposed by static immersion. In contrast, we found that inflammation mediated by chemokine and cytokine signaling pathways was exclusively enriched in the larvae exposed by injection, while the integrin signaling pathway and angiogenesis were solely enriched in the larvae exposed by immersion. We also found important virulence factors from P. aeruginosa that were enriched only after exposure by injection, such as the Type-III secretion system and flagella-associated proteins. On the other hand, P. aeruginosa proteins involved in processes like biofilm formation, cellular responses to antibiotic and starvation were enriched exclusively after an exposure by immersion. We demonstrated the suitability of zebrafish embryos as a model for in vivo Host-Pathogen based proteomic studies in P. aeruginosa. Our global proteomic profiling identifies novel molecular signatures that give systematic insight into zebrafish-Pseudomonas Interaction.

Bryndis Ragnarsdottir - One of the best experts on this subject based on the ideXlab platform.

  • Susceptibility to acute pyelonephritis or asymptomatic bacteriuria: Host–Pathogen Interaction in urinary tract infections
    Pediatric Nephrology, 2012
    Co-Authors: Bryndis Ragnarsdottir, Catharina Svanborg
    Abstract:

    Our knowledge of the molecular mechanisms of urinary tract infection (UTI) Pathogenesis has advanced greatly in recent years. In this review, we provide a general background of UTI Pathogenesis, followed by an update on the mechanisms of UTI susceptibility, with a particular focus on genetic variation affecting innate immunity. The innate immune response of the Host is critically important in the antibacterial defence mechanisms of the urinary tract, and bacterial clearance normally proceeds without sequelae. However, slight dysfunctions in these mechanisms may result in acute disease and tissue destruction. The symptoms of acute pyelonephritis are caused by the innate immune response, and inflammation in the urinary tract decreases renal tubular function and may give rise to renal scarring, especially in paediatric patients. In contrast, in children with asymptomatic bacteriuria (ABU), bacteria persist without causing symptoms or pathology. Pathogenic agents trigger a response determined by their virulence factors, mediating adherence to the urinary tract mucosa, signalling through Toll-like receptors (TLRs) and activating the defence mechanisms. In ABU strains, such virulence factors are mostly not expressed. However, the influence of the Host on UTI severity cannot be overestimated, and rapid progress is being made in clarifying Host susceptibility mechanisms. For example, genetic alterations that reduce TLR4 function are associated with ABU, while polymorphisms reducing IRF3 or CXCR1 expression are associated with acute pyelonephritis and an increased risk for renal scarring. It should be plausible to “individualize” diagnosis and therapy by combining information on bacterial virulence and the Host response.

  • susceptibility to acute pyelonephritis or asymptomatic bacteriuria Host Pathogen Interaction in urinary tract infections
    Pediatric Nephrology, 2012
    Co-Authors: Bryndis Ragnarsdottir, Catharina Svanborg
    Abstract:

    Our knowledge of the molecular mechanisms of urinary tract infection (UTI) Pathogenesis has advanced greatly in recent years. In this review, we provide a general background of UTI Pathogenesis, followed by an update on the mechanisms of UTI susceptibility, with a particular focus on genetic variation affecting innate immunity. The innate immune response of the Host is critically important in the antibacterial defence mechanisms of the urinary tract, and bacterial clearance normally proceeds without sequelae. However, slight dysfunctions in these mechanisms may result in acute disease and tissue destruction. The symptoms of acute pyelonephritis are caused by the innate immune response, and inflammation in the urinary tract decreases renal tubular function and may give rise to renal scarring, especially in paediatric patients. In contrast, in children with asymptomatic bacteriuria (ABU), bacteria persist without causing symptoms or pathology. Pathogenic agents trigger a response determined by their virulence factors, mediating adherence to the urinary tract mucosa, signalling through Toll-like receptors (TLRs) and activating the defence mechanisms. In ABU strains, such virulence factors are mostly not expressed. However, the influence of the Host on UTI severity cannot be overestimated, and rapid progress is being made in clarifying Host susceptibility mechanisms. For example, genetic alterations that reduce TLR4 function are associated with ABU, while polymorphisms reducing IRF3 or CXCR1 expression are associated with acute pyelonephritis and an increased risk for renal scarring. It should be plausible to “individualize” diagnosis and therapy by combining information on bacterial virulence and the Host response.