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Reasonable Similarities Between Opportunistic Bacterial Pathogens: The Curious Case of Haemophilus influenzae and Helicobacter pylori

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Ariadna Fernández-Calvet1Ariadna Fernández-Calvet1Ariadna Fernández-Calvet1,2

1Institute of Agrobiotechnology, CSIC-Gobierno Navarra, Mutilva, Navarra 2Center for Networked Biomedical Research in Respiratory Diseases, Madrid

Ariadna Fernández-Calvet

Group photo. Ariadna Fernández-Calvet

Ariadna Fernández-Calvet et al. 2017). Whole genome sequencing has revealed pathoadaptive genomic traits that, in some cases, are common to opportunistic pathogens that colonize different niches in the same host, leading to . 2017). Whole genome sequencing has revealed pathoadaptive genomic traits that, in some cases, are common to opportunistic pathogens that colonize different niches in the same host, leading to . 2017). Whole genome sequencing has revealed pathoadaptive genomic traits that, in some cases, are common to opportunistic pathogens that colonize different niches in the same host, leading to

. 2017). Whole genome sequencing has revealed pathoadaptive genomic traits that, in some cases, are common to opportunistic pathogens that colonize different niches in the same host, leading to Haemophilus influenzae. 2017). Whole genome sequencing has revealed pathoadaptive genomic traits that, in some cases, are common to opportunistic pathogens that colonize different niches in the same host, leading to et al. 2018). Comparative genomic analysis has revealed the enormous variability that exists between decapsulated isolates of this bacterium, translated into significant phenotypic heterogeneity. The genomic plasticity of In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as . 2018). Comparative genomic analysis has revealed the enormous variability that exists between decapsulated isolates of this bacterium, translated into significant phenotypic heterogeneity. The genomic plasticity of et al. 2018). Comparative genomic analysis has revealed the enormous variability that exists between decapsulated isolates of this bacterium, translated into significant phenotypic heterogeneity. The genomic plasticity of In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as undergoes phase variation, a high-frequency, reversible, stochastic phenomenon determined by the existence of simple-sequence repeats. undergoes phase variation, a high-frequency, reversible, stochastic phenomenon determined by the existence of simple-sequence repeats. undergoes phase variation, a high-frequency, reversible, stochastic phenomenon determined by the existence of simple-sequence repeats. In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as it also presents epigenetic regulation systems regulated by phase variation. Thus, phase variation in genes encoding DNA methyltransferases generates changes in the global methylation pattern, which in turn regulate the global gene expression profile of the pathogen (Phillips et alit also presents epigenetic regulation systems regulated by phase variation. Thus, phase variation in genes encoding DNA methyltransferases generates changes in the global methylation pattern, which in turn regulate the global gene expression profile of the pathogen (Phillips

it also presents epigenetic regulation systems regulated by phase variation. Thus, phase variation in genes encoding DNA methyltransferases generates changes in the global methylation pattern, which in turn regulate the global gene expression profile of the pathogen (Phillips In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as with chromosomal reduction traits. This pathogen lacks a fatty acid β-oxidation pathway, and the uptake of non-metabolizable exogenous fatty acids has a detergent effect, partially alleviated by the inactivation of the gene that encodes the FadL fatty acid transporter. This is a trait of parallel evolution observed in persistent strains isolated from the lung of COPD patients, a niche with high levels of lipid-based inflammatory mediators (Moleres et alwith chromosomal reduction traits. This pathogen lacks a fatty acid β-oxidation pathway, and the uptake of non-metabolizable exogenous fatty acids has a detergent effect, partially alleviated by the inactivation of the gene that encodes the FadL fatty acid transporter. This is a trait of parallel evolution observed in persistent strains isolated from the lung of COPD patients, a niche with high levels of lipid-based inflammatory mediators (Moleres In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as it presents an incomplete Krebs cycle with the absence of the enzymes of the oxidative branch, and it catabolizes glucose through a respiration-assisted fermentation whose main excreted product is acetic acid, which in turn is a proinflammatory immunometabolite. This is a feature of metabolic adaptation in the COPD lung, where glucose availability is high due to the basal inflammation characteristic of the disease (López-López, unpublished data). A final example is the phase variation in the promoter of the gene encoding the adhesin/invasin HMW1/2A. The progressive increase in SSRs associated with the persistence of In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon et alin the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon

in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon Helicobacter pyloriin the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon et alin the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon it is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon it is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, et alit is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, et alit is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, et alit is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon it is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, it is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, it is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, In addition, we have constructed the most potent chimeric enzymes against pneumococcus (Cpl-711 and PL3), strictly specific against this bacterium, but we have also characterized other endolysins with a broader host range, such as Cpl-7S and Csl2. Likewise, we have verified its synergistic action with certain antibiotics, or also between two enzybiotics that break different bonds. All of these enzymes have been shown to be highly effective against susceptible bacteria that form biofilms and have been validated in animal models, such as mice or zebrafish. In addition, we are studying new endolysins against Gram-negative pathogens, such as it is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, et alit is also determined by natural competition and phase variation – including epigenetic regulation of gene expression. Furthermore, both the b-oxidation pathway and the Krebs cycle are incomplete, et al. 2011). Finally, the expression of the surface proteins SabA and BabA, involved in the adhesion of in the COPD lung regulates the progressive decrease in the levels of this protein, a possible trait of natural selection in response to the high titer of anti-HMW1/2A antibodies in the colonized niche (Cholon . 2011). Finally, the expression of the surface proteins SabA and BabA, involved in the adhesion of et al. 2011). Finally, the expression of the surface proteins SabA and BabA, involved in the adhesion of et al. 2011). Finally, the expression of the surface proteins SabA and BabA, involved in the adhesion of

. 2011). Finally, the expression of the surface proteins SabA and BabA, involved in the adhesion of

 

References

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Price LB, Hungate BA, Koch BJ, Davis GS y Liu CM. Price LB, Hungate BA, Koch BJ, Davis GS y Liu CM. Haemophilus influenzaePrice LB, Hungate BA, Koch BJ, Davis GS y Liu CM.

Mell JC Price LB, Hungate BA, Koch BJ, Davis GS y Liu CM. Price LB, Hungate BA, Koch BJ, Davis GS y Liu CM.

Price LB, Hungate BA, Koch BJ, Davis GS y Liu CM. Price LB, Hungate BA, Koch BJ, Davis GS y Liu CM.

Moleres J, Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J . , Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J . Haemophilus influenzae , Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J .

, Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J . , Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J . Haemophilus influenzae , Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J .

, Fernández-Calvet A, Ehrlich RL, Martí S, Pérez-Regidor L, Euba B, Rodríguez-Arce I, Balashov S, Cuevas E, Liñares J, Ardanuy C, Martín-Santamaría S, Ehrlich GD, Mell JC and Garmendia J . S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61.

S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. Helicobacter pylori S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61.

S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61.S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. Helicobacter pyloriS. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61.

S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. Helicobacter pylori S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61.

S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. Haemophilus influenzae S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61.

S. (2013). Survival in hostile territory: the microbiota of the stomach. FEMS Microbiol Rev. 37(5):736-61. (2014). Repetitive sequence variations in the promoter region of the adhesin-encoding gene (2014). Repetitive sequence variations in the promoter region of the adhesin-encoding gene (2014). Repetitive sequence variations in the promoter region of the adhesin-encoding gene Helicobacter pylori (2014). Repetitive sequence variations in the promoter region of the adhesin-encoding gene

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(2014). Repetitive sequence variations in the promoter region of the adhesin-encoding gene Haemophilus influenzae and Helicobacter pylori