ReviewAdvances in experimental medicine and biology2022
Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.
Review in Advances in experimental medicine and biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Landscape of resistance to ceftolozane/tazobactam and ceftazidime/avibactam in strains of Pseudomonas aeruginosa: a genomic approach in strains without selection pressure in a tertiary-care paediatric hospital in Mexico.BMC infectious diseases · 2026Article
- Growth in Anaerobic Bottles is an Independent Predictor of Mortality in Pseudomonas aeruginosa Bloodstream Infections.Infectious diseases and therapy · 2026Article
- High frequency body site translocation of nosocomial Pseudomonas aeruginosa.Nature communications · 2025Article
- Strain-specific variation in the complement resistome ofInfection and immunity · 2025Article
- Impact of the COVID-19 pandemic on the epidemiology and molecular features of Pseudomonas aeruginosa bloodstream infections.Scientific reports · 2025Article
- Bloodstream infections: mechanisms of pathogenesis and opportunities for intervention.Nature reviews. Microbiology · 2025Review
- Novel broadly reactive monoclonal antibody protects againstInfection and immunity · 2025Article
- Article
- Cleavage of cell junction proteins as a host invasion strategy in leptospirosis.Applied microbiology and biotechnology · 2024Review
- Fitness factor genes conserved within the multi-species core genome of Gram-negative Enterobacterales species contribute to bacteremia pathogenesis.PLoS pathogens · 2024Article
- ModifiedFrontiers in molecular biosciences · 2023Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bloodstream infections (BSI) with Pseudomonas aeruginosa account for 8.5% of all BSIs, their mortality rate, at about 40%, is the highest among causative agents. For this reason and due to its intrinsic and acquired resistance to antibiotics, P. aeruginosa represents a threat to public health systems. From the primary site of infection, often the urinary and respiratory tracts, P. aeruginosa uses its arsenal of virulence factors to cross both epithelial and endothelial barriers, ultimately reaching the bloodstream. In this chapter, we review the main steps involved in invasion and migration of P. aeruginosa into blood vessels, and the molecular mechanisms governing bacterial survival in blood. We also review the lifestyle of P. aeruginosa "on" and "in" host cells. In the context of genomic and phenotypic diversity of laboratory strains and clinical isolates, we underline the need for more standardized and robust methods applied to host-pathogen interaction studies, using several representative strains from distinct phylogenetic groups before drawing general conclusions. Finally, our literature survey reveals a need for further studies to complete our comprehension of the complex interplay between P. aeruginosa and the immune system in the blood, specifically in relation to the complement system cascade(s) and the Membrane Attack Complex (MAC), which play crucial roles in counteracting P. aeruginosa BSI.
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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.