ArticleSub-cellular biochemistry2010
The role of Pseudomonas lipopolysaccharide in cystic fibrosis airway infection.
Article in Sub-cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 62 citations in OpenAlex.
- Transposon insertion sequencing of Pseudomonas aeruginosa identifies multiple intersecting pathways essential for extreme colistin resistance.PLoS pathogens · 2026Article
- Engineering low-endotoxin lipid A in a double auxotrophFrontiers in cellular and infection microbiology · 2026Article
- Genomic and phenotypic insight into antimicrobial resistance ofFrontiers in microbiology · 2025Article
- Understanding the pathophysiology ofBurns & trauma · 2025Review
- Article
- Lipoarabinomannan modification as a source of phenotypic heterogeneity in host-adaptedProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Antimicrobial peptide glatiramer acetate targets Pseudomonas aeruginosa lipopolysaccharides to breach membranes without altering lipopolysaccharide modification.npj antimicrobials and resistance · 2024Article
- DivergentmBio · 2024Article
- Mutations in genesAntimicrobial agents and chemotherapy · 2024Article
- Genomic and Functional Characterization of Longitudinal Pseudomonas aeruginosa Isolates from Young Patients with Cystic Fibrosis.Microbiology spectrum · 2023Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Loss of RND-Type Multidrug Efflux Pumps Triggers Iron Starvation and Lipid A Modifications in Pseudomonas aeruginosa.Antimicrobial agents and chemotherapy · 2021Article
- Specific and Global RNA Regulators inInternational journal of molecular sciences · 2021Review
- Defining the Mechanistic Correlates of Protection Conferred by Whole-Cell Vaccination against Pseudomonas aeruginosa Acute Murine Pneumonia.Infection and immunity · 2021Article
- On-Tissue Derivatization of Lipopolysaccharide for Detection of Lipid A Using MALDI-MSI.Analytical chemistry · 2020Article
- The Anti-Microbial Peptide (Lin-SB056-1)Antibiotics (Basel, Switzerland) · 2020Article
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- A Screen for Antibiotic Resistance Determinants Reveals a Fitness Cost of the Flagellum in Pseudomonas aeruginosa.Journal of bacteriology · 2020Article
- Steering Phages to Combat Bacterial Pathogens.Trends in microbiology · 2020Review
- Profiling the susceptibility of Pseudomonas aeruginosa strains from acute and chronic infections to cell-wall-targeting immune proteins.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa (PA) is a ubiquitous environmental Gram-negative bacterium found in soil and water. This opportunistic pathogen can cause infections in individuals with impaired phagocytic function, such as those with burns, exposure to chemotherapy, or cystic fibrosis (CF). PA infects the lungs of most individuals with CF, and is associated with severe progressive pulmonary disease that is the major cause of premature death in this disorder. The specific adaptations of PA to the CF airway responsible for bacterial persistence and antibiotic tolerance are not completely understood but may include increased alginate production (i.e., mucoid phenotype), biofilm formation, and specific lipid A modifications. During adaptation to the CF airway, PA synthesizes a variety of lipid A structures that alter host innate immune responses and promote bacterial persistence and chronic infection. The synthesis of specific lipid A structures is attributable to bacterial enzymes that: (1) remove the 3OH-C10:0 acyl chain from the 3-position (PagL); (2) add a C16:0 acyl chain to the 3OH-C10:0 chain at the 3'-position (PagP); (3) add C12:0 and 2OH-C12:0 acyl chains to the 3OH-C12:0 chains at the 2- and 2'-positions (HtrB and LpxO); and (4) add aminoarabinose to phosphate groups at the 1- and 4'-positions (PmrH, PmrF, PmrI, PmrJ, PmrK, and PmrE). These lipid A modifications represent an essential aspect of PA adaptation to the CF airway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.