Bacterial Pathogens-Host Interface in Cystic Fibrosis

Dear Colleagues,

Cystic Fibrosis (CF) is a genetic disorder that primarily affects the lungs and digestive system, but also the pancreas, liver, and kidney. CF is an inherited disease in an autosomal recessive manner. It is caused by the presence of diverse mutations in one or both copies of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR protein is a chloride channel involved in the regulation of chloride ion content of epithelial cells associated with the nasal cavity, lungs, and stomach. A malfunction of CFTR leads to a reduction in the epithelial cells to move chloride out, and therefore, the inability of the lungs to retain water and moisture. The lungs of people with CF develop a thick and sticky layer of mucus, which several bacterial pathogens can colonize. People with CF and bacterial infections are commonly treated with antibiotics that are provided intravenously or by inhaled pathways. The most frequent bacterial pathogens associated with CF are Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa. In addition to the defined typically bacterial pathogens, CF patients with frequency are also infected with Burkholderia cenocepacia, Stenotrophomonas maltophilia and nontuberculous Mycobacteria. During the life of people with CF, Staphylococcus aureus is considered the first pathogen that infects and colonizes the airways of these patients, which cause epithelial damage, opening the way to other opportunistic pathogens such as Pseudomonas aeruginosa. This pathogen is the most prevalent bacteria that colonize the lungs of people with CF and persist until the end of their lives. Methicillin-resistant S. aureus (MRSA) has become the most important nosocomial pathogen that rapidly increased its prevalence in CF patients.

In the lungs, these pathogens survive into polymicrobial communities in which they compete for a place and nutrients through specific regulation of the expression of several virulence factors. Bacterial detection by the host produces inflammation and recruitment of innate immune cells. In this context, the inability of innate immune cells to clear bacteria from the lungs results in bacterial persistence, which maintain inflammatory signals and chronic infections leading to rapid decline in the lung function and the increased risk in morbidity and mortality.

This Research Topic aims to improve our understanding of the mechanisms at the host–pathogen interface used by bacteria to colonize the lungs of people with CF, to promote tissue damage and to avert innate and adaptative immune responses by the host.

The specific areas of interest in the context of CF include (but are not limited to):

• The identification of virulence factors involved in bacterial attachment, invasion and survival on phagocytic and non-phagocytic cells
• Mechanisms involved in the induction of inflammatory immune responses.
• Contribution of the host immune response to bacterial clearance
• Dysfunctional immune responses to bacterial pathogens
• Interactions between distinct bacterial pathogens in the lungs
• Mechanisms of bacterial adaptation to lung environment
• Strategies to combat recalcitrant bacterial infections
• New strategies to kill bacteria or modulate the CFTR function

In this research topic we welcome the contribution of original research articles as well as reviews on the field.

Dr. Roberto Rosales-Reyes
Guest Editor

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• cystic fibrosis
• bacterial pathogens
• bacterial adaptation
• bacterial pathogenesis
• cell–host interaction
• immune response
• modulators effect, antimicrobial resistance