Interaction among variants in the SLC gene family (SLC6A14 , SLC26A9 , SLC11A1 , and SLC9A3 ) and CFTR mutations with clinical markers of cystic fibrosis – ScienceOpen
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      Interaction among variants in the SLC gene family (SLC6A14 , SLC26A9 , SLC11A1 , and SLC9A3 ) and CFTR mutations with clinical markers of cystic fibrosis

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          Pseudomonas aeruginosa Lifestyle: A Paradigm for Adaptation, Survival, and Persistence

          Pseudomonas aeruginosa is an opportunistic pathogen affecting immunocompromised patients. It is known as the leading cause of morbidity and mortality in cystic fibrosis (CF) patients and as one of the leading causes of nosocomial infections. Due to a range of mechanisms for adaptation, survival and resistance to multiple classes of antibiotics, infections by P. aeruginosa strains can be life-threatening and it is emerging worldwide as public health threat. This review highlights the diversity of mechanisms by which P. aeruginosa promotes its survival and persistence in various environments and particularly at different stages of pathogenesis. We will review the importance and complexity of regulatory networks and genotypic-phenotypic variations known as adaptive radiation by which P. aeruginosa adjusts physiological processes for adaptation and survival in response to environmental cues and stresses. Accordingly, we will review the central regulatory role of quorum sensing and signaling systems by nucleotide-based second messengers resulting in different lifestyles of P. aeruginosa. Furthermore, various regulatory proteins will be discussed which form a plethora of controlling systems acting at transcriptional level for timely expression of genes enabling rapid responses to external stimuli and unfavorable conditions. Antibiotic resistance is a natural trait for P. aeruginosa and multiple mechanisms underlying different forms of antibiotic resistance will be discussed here. The importance of each mechanism in conferring resistance to various antipseudomonal antibiotics and their prevalence in clinical strains will be described. The underlying principles for acquiring resistance leading pan-drug resistant strains will be summarized. A future outlook emphasizes the need for collaborative international multidisciplinary efforts to translate current knowledge into strategies to prevent and treat P. aeruginosa infections while reducing the rate of antibiotic resistance and avoiding the spreading of resistant strains.
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            Pseudomonas aeruginosa Evolutionary Adaptation and Diversification in Cystic Fibrosis Chronic Lung Infections

            Pseudomonas aeruginosa populations undergo a characteristic evolutionary adaptation during chronic infection of the cystic fibrosis (CF) lung, including reduced production of virulence factors, transition to a biofilm-associated lifestyle, and evolution of high-level antibiotic resistance. Populations of P. aeruginosa in chronic CF lung infections typically exhibit high phenotypic diversity, including for clinically important traits such as antibiotic resistance and toxin production, and this diversity is dynamic over time, making accurate diagnosis and treatment challenging. Population genomics studies reveal extensive genetic diversity within patients, including for transmissible strains the coexistence of highly divergent lineages acquired by patient-to-patient transmission. The inherent spatial structure and spatial heterogeneity of selection in the CF lung appears to play a key role in driving P. aeruginosa diversification.
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                Author and article information

                Journal
                Pediatric Pulmonology
                Pediatr Pulmonol
                Wiley
                87556863
                July 2018
                July 2018
                April 10 2018
                : 53
                : 7
                : 888-900
                Affiliations
                [1 ]Department of Medical Genetics, School of Medical Sciences; University of Campinas; Campinas São Paulo Brazil
                [2 ]Department of Pediatrics, School of Medical Sciences; University of Campinas; Campinas São Paulo Brazil
                [3 ]Laboratory of Pulmonary Physiology, Center for Pediatrics Investigation, School of Medical Sciences; University of Campinas; Campinas São Paulo Brazil
                Article
                10.1002/ppul.24005
                f2337c18-e2a1-4bf7-9ab6-1fdc068bbbab
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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