Cystic fibrosis

Mayo Clinic overview

NIH

Pseudomonal infection in cystic fibrosis: the battle continues.¹⁾

Pseudomonas aeruginosa lung infection is the major cause of morbidity and mortality in patients with cystic fibrosis. Infection usually begins in childhood and is responsible for respiratory failure and death in most patients with cystic fibrosis. The organism triggers an exuberant chronic inflammatory reaction which damages the airways and leads to progressive loss of lung function.

This review provides an overview of pseudomonal infection in cystic fibrosis, including mechanisms by which the bacteria may colonize the cystic fibrosis airway, persistence of pseudomonal infection and the biofilm A structured community of microorganisms encapsulated within a self-developed protective matrix and living together. mode of growth. Available treatments and possible novel approaches to therapy will be discussed.

Evolution of airway microbiology in the infant with cystic fibrosis: role of nonpseudomonal and pseudomonal pathogens.²⁾

Bacterial colonization of the airways of the infant with cystic fibrosis is usually established early in life, and, once established, is difficult to eradicate and is associated with progressive lung disease.

Recent research on risk factors for early Pseudomonas aeruginosa colonization, including the potential role of respiratory viral infections, is discussed. We conclude with a discussion of the role of prophylactic antibiotic therapy.

ChIP-seq reveals the global regulator AlgR mediating cyclic di-GMP synthesis in Pseudomonas aeruginosa ³⁾

AlgR is a key transcriptional regulator required for the expression of multiple virulence factors, including type IV pili and alginate in Pseudomonas aeruginosa.

A ΔalgR strain produced lesser biofilm than did the wild-type strain, which is consistent with a phenotype controlled by c-di-GMP.

Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients. ⁴⁾

The concomitant development of QS malfunction significantly correlated with the reduced production of rhamnolipids and elastase and with the occurrence of mutations in the regulatory genes lasR and rhlR.