Antimicrobial resistance (AMR) poses a significant threat to global public health. With the emergence of new resistant strains and limited antibiotic treatment options, it has become increasingly difficult to treat infections effectively. This is particularly concerning for bacterial infections like Mycobacterium tuberculosis, Acinetobacter spp., Staphylococcus aureus, and Pseudomonas aeruginosa, where only a limited number of antibiotics are available for treatment. According to the US National Strategy for Combating Antibiotic-Resistant Bacteria, approximately 2 million Americans are infected with antibiotic-resistant bacteria each year, and at least 23,000 die as a result. The situation is even worse in developing countries.
Systems biology, which aims to understand the complex interactions between the different components of a biological system, has emerged as a powerful tool for studying AMR. By integrating data from multiple sources, including genomics, transcriptomics, proteomics, and metabolomics, systems biology can provide a comprehensive view of the mechanisms underlying AMR. This approach can lead to the identification of novel targets for drug development and the development of personalized treatment strategies that consider the specific characteristics of individual patients and the pathogens that infect them. This Research Topic aims to explore the potential of systems biology in combating antibiotic resistance, and highlight the need for further research to fully realize its clinical potential in infectious diseases.
This Research Topic will to highlight the critical issue of antimicrobial resistance in bacteria and explore the potential of systems biology in identifying new drug targets and combatting AMR, particularly in Mycobacterium tuberculosis, Acinetobacter spp., Staphylococcus aureus, and Pseudomonas aeruginosa infections. This collection will also discuss how the critical cellular changes associated with AMR resistance, such as energy production, cell wall modifications, and cellular interactions, can be targeted using systems biology. Additionally, it will explore how systems biology can capture host metabolites that can target host pathways or help diagnose infectious diseases.
The Research Topic will emphasize the need for further research to fully realize the clinical potential of systems biology in infectious diseases. The insights from the published articles will be valuable for scientists, clinicians, and policymakers working towards the development of new strategies to combat AMR. Particularly, Original Research and Review article are welcome concerning the below mention themes:
• Non-antibiotic treatment targeting various metabolic pathways;
• Identification of genomic signatures and biomarkers for infectious disease;
• Microbiota-derived metabolites and their role in infectious disease and AMR;
• System biology-based approaches to understand and control AMR;
• Host directed systems biology to develop sustainable therapies;
• Microbial system level modeling and novel drug discoveries.
Antimicrobial resistance (AMR) poses a significant threat to global public health. With the emergence of new resistant strains and limited antibiotic treatment options, it has become increasingly difficult to treat infections effectively. This is particularly concerning for bacterial infections like Mycobacterium tuberculosis, Acinetobacter spp., Staphylococcus aureus, and Pseudomonas aeruginosa, where only a limited number of antibiotics are available for treatment. According to the US National Strategy for Combating Antibiotic-Resistant Bacteria, approximately 2 million Americans are infected with antibiotic-resistant bacteria each year, and at least 23,000 die as a result. The situation is even worse in developing countries.
Systems biology, which aims to understand the complex interactions between the different components of a biological system, has emerged as a powerful tool for studying AMR. By integrating data from multiple sources, including genomics, transcriptomics, proteomics, and metabolomics, systems biology can provide a comprehensive view of the mechanisms underlying AMR. This approach can lead to the identification of novel targets for drug development and the development of personalized treatment strategies that consider the specific characteristics of individual patients and the pathogens that infect them. This Research Topic aims to explore the potential of systems biology in combating antibiotic resistance, and highlight the need for further research to fully realize its clinical potential in infectious diseases.
This Research Topic will to highlight the critical issue of antimicrobial resistance in bacteria and explore the potential of systems biology in identifying new drug targets and combatting AMR, particularly in Mycobacterium tuberculosis, Acinetobacter spp., Staphylococcus aureus, and Pseudomonas aeruginosa infections. This collection will also discuss how the critical cellular changes associated with AMR resistance, such as energy production, cell wall modifications, and cellular interactions, can be targeted using systems biology. Additionally, it will explore how systems biology can capture host metabolites that can target host pathways or help diagnose infectious diseases.
The Research Topic will emphasize the need for further research to fully realize the clinical potential of systems biology in infectious diseases. The insights from the published articles will be valuable for scientists, clinicians, and policymakers working towards the development of new strategies to combat AMR. Particularly, Original Research and Review article are welcome concerning the below mention themes:
• Non-antibiotic treatment targeting various metabolic pathways;
• Identification of genomic signatures and biomarkers for infectious disease;
• Microbiota-derived metabolites and their role in infectious disease and AMR;
• System biology-based approaches to understand and control AMR;
• Host directed systems biology to develop sustainable therapies;
• Microbial system level modeling and novel drug discoveries.