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Chronic Lung Infection (chronic + lung_infection)
Selected AbstractsNovel conjugate vaccine for the prevention of Pseudomonas aeruginosa infection in cystic fibrosis patientsDRUG DEVELOPMENT RESEARCH, Issue 8 2007Kelly L. Matson Abstract The published literature evaluating the safety and immunogenicity of the polyvalent O-polysaccharide-toxin A conjugate vaccine is reviewed. Primary immunization followed by annual booster significantly reduced the incidence of chronic Pseudomonas aeruginosa lung infections (particularly mucoid phenotype strains) and extended time to infection. The findings reflected lower frequency of P. aeruginosa in sputum/throat cultures and preservation of lung function. Additionally, studies indicated higher binding affinity of vaccine-induced anti-lipopolysaccharide (LPS) compared with infection-induced anti-LPS serum immunoglobulin G antibodies, suggesting protective capacity. P. aeruginosa prophylaxis with the conjugate vaccine in cystic fibrosis patients has proved safe and useful in preventing and delaying chronic lung infection. Drug Dev Res 68:512,521, 2007. © 2008 Wiley-Liss, Inc. [source] Proteome analysis reveals adaptation of Pseudomonas aeruginosa to the cystic fibrosis lung environmentPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 14 2005Dinesh Diraviam Sriramulu Abstract Pseudomonas aeruginosa is known for the chronic lung colonization of cystic fibrosis (CF) patients in addition to eye, ear and urinary tract infections. With the underlying disease CF patients are predisposed to P.,aeruginosa chronic lung infection, which leads to morbidity and mortality. In this study, we compared the protein expression profile of a CF lung-adapted P.,aeruginosa strain C with that of the burn-wound isolate PAO. Differentially expressed proteins from the whole-cell, membrane, periplasmic as well as extracellular fraction were identified. The whole-cell proteome of strain C showed down-regulation of several proteins involved in amino acid metabolism, fatty acid metabolism, energy metabolism and adaptation leading to a highly distinct proteome pattern for strain C in comparison to PAO. Analysis of secreted proteins by strain C compared to PAO revealed differential expression of virulence factors under non-inducing conditions. The membrane proteome of strain C showed modulation of the expression of porins involved in nutrient and antibiotic influx. The proteome of the periplasmic space of strain C showed retention of elastase despite that the equal amounts were secreted by strain C and PAO. Altogether, our results elucidate adaptive strategies of P.,aeruginosa towards the nutrient-rich CF lung habitat during the course of chronic colonization. [source] Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host,pathogen interactions in cystic fibrosisAPMIS, Issue 2 2009CLAUS MOSER The dominant cause of premature death in patients suffering from cystic fibrosis (CF) is chronic lung infection with Pseudomonas aeruginosa. The chronic lung infection often lasts for decades with just one clone. However, as a result of inflammation, antibiotic treatment and different niches in the lungs, the clone undergoes significant genetic changes, resulting in diversifying geno- and phenotypes. Such an adaptation may generate different host responses. To experimentally reflect the year-long chronic lung infection in CF, groups of BALB/c mice were infected with clonal isolates from different periods (1980, 1988, 1997, 1999 and 2003) of the chronic lung infection of one CF patient using the seaweed alginate embedment model. The results showed that the non-mucoid clones reduced their virulence over time, resulting in faster clearing of the bacteria from the lungs, improved pathology and reduced pulmonary production of macrophage inflammatory protein-2 (MIP-2) and granulocyte colony-stimulating factor (G-CSF). In contrast, the mucoid clones were more virulent and virulence increased with time, resulting in impaired pulmonary clearing of the latest clone, severe inflammation and increased pulmonary MIP-2 and G-CSF production. In conclusion, adaptation of P. aeruginosa in CF is reflected by changed ability to establish lung infection and results in distinct host responses to mucoid and non-mucoid phenotypes. [source] | ||||||||||