Role of Host and Bacterial Lipids in Pseudomonas aeruginosa Respiratory Infections

Abstract

The opportunistic pathogen Pseudomonas aeruginosa is one of the most common agents of respiratory infections and has been associated with high morbidity and mortality rates. The ability of P. aeruginosa to cause severe respiratory infections results from the coordinated action of a variety of virulence factors that promote bacterial persistence in the lungs. Several of these P. aeruginosa virulence mechanisms are mediated by bacterial lipids, mainly lipopolysaccharide, rhamnolipid, and outer membrane vesicles. Other mechanisms arise from the activity of P. aeruginosa enzymes, particularly ExoU, phospholipase C, and lipoxygenase A, which modulate host lipid signaling pathways. Moreover, host phospholipases, such as cPLA2α and sPLA2, are also activated during the infectious process and play important roles in P. aeruginosa pathogenesis. These mechanisms affect key points of the P. aeruginosa-host interaction, such as: i) biofilm formation that contributes to bacterial colonization and survival, ii) invasion of tissue barriers that allows bacterial dissemination, iii) modulation of inflammatory responses, and iv) escape from host defenses. In this mini-review, we present the lipid-based mechanism that interferes with the establishment of P. aeruginosa in the lungs and discuss how bacterial and host lipids can impact the outcome of P. aeruginosa respiratory infections.

Lactobacillus Probiotic Strains Differ in Their Ability to Adhere to Human Lung Epithelial Cells and to Prevent Adhesion of Clinical Isolates of Pseudomonas aeruginosa from Cystic Fibrosis Lung

“…According to FAO/WHO guidelines, besides having the ability to adhere to epithelial cells, potential probiotics strains must exhibit antagonistic properties against pathogenic microorganisms [ 30 ]. P. aeruginosa is a major respiratory pathogen [ 31 ]. In CF patients, in particular, its prevalence ranges from 10 to 30% at ages 0–5, increasing up to 80% at age ≥ 18 years [ 32 ].…”

Quorum-Sensing Signaling Molecule 2-Aminoacetophenone Mediates the Persistence of Pseudomonas aeruginosa in Macrophages by Interference with Autophagy through Epigenetic Regulation of Lipid Biosynthesis

“…For example, oleate was shown to protect Caenorhabditis elegans from this pathogen’s infection ( 50 ). In addition, P. aeruginosa enzymes, including phospholipase C, lipoxygenase A, and ExoU, have been reported to impact host lipid pathways in the lung epithelial cells ( 51 ). The P. aeruginosa QS autoinducer N-3-oxo-dodecanoyl homoserine lactone has been reported to change the membrane dipole potential in lymphocytes by accumulating in the cholesterol-containing microdomains, leading to membrane conformation changes that impact immune signaling ( 52 ).…”

Metabolic Changes in Pseudomonas oleovorans Isolated from Contaminated Construction Material Exposed to Varied Biocide Treatments

“…When microbes are exposed to various types of biocides, this can lead to alterations in metabolism. This response is due to the multi-targeted antimicrobial action of biocides, which can affect the cellular structures and functions of microorganisms [26,27]. These changes are often indicative of the organism's response to stress or environmental disturbance [28].…”