Abstract
Cystic fibrosis (CF) is the most common lethal inherited disorder in Caucasians. It is caused by mutation of the CF transmembrane conductance regulator (CFTR) gene. A defect in the CFTR ion channel causes a dramatic change in the composition of the airway surface fluid, leading to a highly viscous mucus layer. In healthy individuals, the majority of bacteria trapped in the mucus layer are removed and destroyed by mucociliary clearance. However, in the lungs of patients with CF, the mucociliary clearance is impaired due to dehydration of the airway surface fluid. As a consequence, patients with CF are highly susceptible to chronic or intermittent pulmonary infections, often causing extensive lung inflammation and damage, accompanied by a decreased life expectancy. This mini review will focus on the different secretion mechanisms used by the major bacterial CF pathogens to release virulence factors, their role in resistance and discusses the potential for therapeutically targeting secretion systems.
Highlights
Protein Secretion by Cystic fibrosis (CF) PathogensCommon to all these species is their dramatic intrinsic or acquired resistance against most of the currently employed antibiotics, making these infections extremely difficult to eradicate
Laboratory for Protein Biochemistry and Biomolecular Engineering, Department of Biochemistry and Microbiology, Ghent University, Ghent, Belgium
Patients with Cystic fibrosis (CF) are highly susceptible to chronic or intermittent pulmonary infections, often causing extensive lung inflammation and damage, accompanied by a decreased life expectancy. This mini review will focus on the different secretion mechanisms used by the major bacterial CF pathogens to release virulence factors, their role in resistance and discusses the potential for therapeutically targeting secretion systems
Summary
Common to all these species is their dramatic intrinsic or acquired resistance against most of the currently employed antibiotics, making these infections extremely difficult to eradicate. Biofilm formation, decreased outer membrane permeability, and inactivation of β-lactam antibiotics by chromosomally encoded β-lactamases are the main causes of resistance (Hoyle and Costerton, 1991; Waters, 2012)
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