Cystic fibrosis (CF) is the most common inherited disease in the Caucasian population with approximately 70,000 patients affected worldwide. This disease is linked to a mutation in the cftr gene, resulting in alteration of the CFTR protein, a chloride channel located at the apical site of epithelial cells in many organs. At the pulmonary level, the mutation is responsible for the presence of viscous mucus which inhibits ciliary beat. The modification of the pulmonary environment and the alteration of mucociliary clearance promote the implantation and multiplication of specific pathogens linked to cystic fibrosis and thus cause a modification of the pulmonary microbiota. Chronic bacterial respiratory infections in patients with cystic fibrosis are responsible for progressive lung disease with exacerbations and bronchiectasis leading to morbidity and mortality with a reduced life expectancy of 46 years. It is estimated that 80% of deaths are due to bacterial infections of the lungs.
The clinical consequences of polymicrobial infections are of major interest. Understanding the
mechanisms of microbial interactions and their clinical relevance is essential to rationally orient current therapies and to develop improved treatments for respiratory infections. Deciphering the impact of co-infection and microbial interactions on the host response at the cellular and molecular levels remains a largely unexplored field. The same is true for the role and impact of polymicrobial infections on the evolution and adaptation of pathogens in this context of chronic infection / colonization.
This Research Topic aims to bring together all types of articles hosted in the journal (Original Research, Methods, Reviews, Mini-Reviews and Perspective articles). The submission can cover any of the following topics:
- Microbiome and diversity of infections in cystic fibrosis
- Diversity and evolution / adaptation of pathogens
- Resistance to antibiotics associated with co-infection
- Clinical consequences of coinfection
- Molecular mechanisms of pathogenic interactions
Cystic fibrosis (CF) is the most common inherited disease in the Caucasian population with approximately 70,000 patients affected worldwide. This disease is linked to a mutation in the cftr gene, resulting in alteration of the CFTR protein, a chloride channel located at the apical site of epithelial cells in many organs. At the pulmonary level, the mutation is responsible for the presence of viscous mucus which inhibits ciliary beat. The modification of the pulmonary environment and the alteration of mucociliary clearance promote the implantation and multiplication of specific pathogens linked to cystic fibrosis and thus cause a modification of the pulmonary microbiota. Chronic bacterial respiratory infections in patients with cystic fibrosis are responsible for progressive lung disease with exacerbations and bronchiectasis leading to morbidity and mortality with a reduced life expectancy of 46 years. It is estimated that 80% of deaths are due to bacterial infections of the lungs.
The clinical consequences of polymicrobial infections are of major interest. Understanding the
mechanisms of microbial interactions and their clinical relevance is essential to rationally orient current therapies and to develop improved treatments for respiratory infections. Deciphering the impact of co-infection and microbial interactions on the host response at the cellular and molecular levels remains a largely unexplored field. The same is true for the role and impact of polymicrobial infections on the evolution and adaptation of pathogens in this context of chronic infection / colonization.
This Research Topic aims to bring together all types of articles hosted in the journal (Original Research, Methods, Reviews, Mini-Reviews and Perspective articles). The submission can cover any of the following topics:
- Microbiome and diversity of infections in cystic fibrosis
- Diversity and evolution / adaptation of pathogens
- Resistance to antibiotics associated with co-infection
- Clinical consequences of coinfection
- Molecular mechanisms of pathogenic interactions