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Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis

Cystic fibrosis (CF) is an autosomal recessive genetic disorder that is characterized by recurrent and chronic infections of the lung predominantly by the opportunistic pathogens, Gram-positive Staphylococcus aureus and Gram-negative Pseudomonas aeruginosa. While S. aureus is the main colonizing bac...

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Autores principales: Biswas, Lalitha, Götz, Friedrich
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8770549/
https://www.ncbi.nlm.nih.gov/pubmed/35071057
http://dx.doi.org/10.3389/fcimb.2021.824042
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author Biswas, Lalitha
Götz, Friedrich
author_facet Biswas, Lalitha
Götz, Friedrich
author_sort Biswas, Lalitha
collection PubMed
description Cystic fibrosis (CF) is an autosomal recessive genetic disorder that is characterized by recurrent and chronic infections of the lung predominantly by the opportunistic pathogens, Gram-positive Staphylococcus aureus and Gram-negative Pseudomonas aeruginosa. While S. aureus is the main colonizing bacteria of the CF lungs during infancy and early childhood, its incidence declines thereafter and infections by P. aeruginosa become more prominent with increasing age. The competitive and cooperative interactions exhibited by these two pathogens influence their survival, antibiotic susceptibility, persistence and, consequently the disease progression. For instance, P. aeruginosa secretes small respiratory inhibitors like hydrogen cyanide, pyocyanin and quinoline N-oxides that block the electron transport pathway and suppress the growth of S. aureus. However, S. aureus survives this respiratory attack by adapting to respiration-defective small colony variant (SCV) phenotype. SCVs cause persistent and recurrent infections and are also resistant to antibiotics, especially aminoglycosides, antifolate antibiotics, and to host antimicrobial peptides such as LL-37, human β-defensin (HBD) 2 and HBD3; and lactoferricin B. The interaction between P. aeruginosa and S. aureus is multifaceted. In mucoid P. aeruginosa strains, siderophores and rhamnolipids are downregulated thus enhancing the survival of S. aureus. Conversely, protein A from S. aureus inhibits P. aeruginosa biofilm formation while protecting both P. aeruginosa and S. aureus from phagocytosis by neutrophils. This review attempts to summarize the current understanding of the molecular mechanisms that drive the competitive and cooperative interactions between S. aureus and P. aeruginosa in the CF lungs that could influence the disease outcome.
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spelling pubmed-87705492022-01-21 Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis Biswas, Lalitha Götz, Friedrich Front Cell Infect Microbiol Cellular and Infection Microbiology Cystic fibrosis (CF) is an autosomal recessive genetic disorder that is characterized by recurrent and chronic infections of the lung predominantly by the opportunistic pathogens, Gram-positive Staphylococcus aureus and Gram-negative Pseudomonas aeruginosa. While S. aureus is the main colonizing bacteria of the CF lungs during infancy and early childhood, its incidence declines thereafter and infections by P. aeruginosa become more prominent with increasing age. The competitive and cooperative interactions exhibited by these two pathogens influence their survival, antibiotic susceptibility, persistence and, consequently the disease progression. For instance, P. aeruginosa secretes small respiratory inhibitors like hydrogen cyanide, pyocyanin and quinoline N-oxides that block the electron transport pathway and suppress the growth of S. aureus. However, S. aureus survives this respiratory attack by adapting to respiration-defective small colony variant (SCV) phenotype. SCVs cause persistent and recurrent infections and are also resistant to antibiotics, especially aminoglycosides, antifolate antibiotics, and to host antimicrobial peptides such as LL-37, human β-defensin (HBD) 2 and HBD3; and lactoferricin B. The interaction between P. aeruginosa and S. aureus is multifaceted. In mucoid P. aeruginosa strains, siderophores and rhamnolipids are downregulated thus enhancing the survival of S. aureus. Conversely, protein A from S. aureus inhibits P. aeruginosa biofilm formation while protecting both P. aeruginosa and S. aureus from phagocytosis by neutrophils. This review attempts to summarize the current understanding of the molecular mechanisms that drive the competitive and cooperative interactions between S. aureus and P. aeruginosa in the CF lungs that could influence the disease outcome. Frontiers Media S.A. 2022-01-06 /pmc/articles/PMC8770549/ /pubmed/35071057 http://dx.doi.org/10.3389/fcimb.2021.824042 Text en Copyright © 2022 Biswas and Götz https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular and Infection Microbiology
Biswas, Lalitha
Götz, Friedrich
Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis
title Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis
title_full Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis
title_fullStr Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis
title_full_unstemmed Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis
title_short Molecular Mechanisms of Staphylococcus and Pseudomonas Interactions in Cystic Fibrosis
title_sort molecular mechanisms of staphylococcus and pseudomonas interactions in cystic fibrosis
topic Cellular and Infection Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8770549/
https://www.ncbi.nlm.nih.gov/pubmed/35071057
http://dx.doi.org/10.3389/fcimb.2021.824042
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