ArticleLipids2014
Analysis of Pseudomonas aeruginosa PAO1 lipid A changes during the interaction with model organism, Caenorhabditis elegans.
Article in Lipids, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Host TGF-β signalling facilitates Vi-capsule mediated adaptive immune evasion and vertical transmission ofCell surface (Amsterdam, Netherlands) · 2025Article
- Ovalbumin promotes innate immune response of Caenorhabditis elegans through DAF-16 and SKN-1 pathways in insulin/IGF-1 signaling.Journal of physiology and biochemistry · 2024Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) is the main surface constituent of Gram-negative bacteria. Lipid A, the hydrophobic moiety, outer monolayer of the outer cell membrane forms the major component of LPS. Immunogenic Lipid A is recognized by the innate immune system through the TLR 4/MD-2 complex. Pseudomonas aeruginosa PAO1, a Gram-negative bacterium is known to cause nosocomial infection and known for its adaptation to adverse environmental conditions. Pseudomonas aeruginosa can infect a broad host spectrum including Caenorhabditis elegans, a simple free living soil nematode. Here, we reveal that PAO1 modifies its Lipid A during the host interaction with C. elegans. The penta-acylated form of Lipid A was identified by using matrix assisted laser desorption ionization-time of flight analysis and the β-(1,6)-linked disaccharide of glucosamine with phosphate groups, 2 and 2' amide linked fatty acid chain and 3 and 3' ester linked fatty acids were investigated for the modification using the non destructive (1)H NMR, spin-lattice (T₁) relaxation measurement, differential scanning calorimetry. T₁ relaxation measurements showed that the 2 and 2' amide linked fatty acid chain, -CH in the glucosamine disaccharide of PAO1 lipid A, in an exposed host had a different spin lattice relaxation time compared to an unexposed host and the findings were reconfirmed using in vitro human corneal epithelial cells cell lines. Furthermore, scanning electron microscope and confocal laser scanning microscopy analysis revealed that the P. aeruginosa PAO1 biofilm formation was disturbed in the exposed host condition. The daf-12, daf-16, tol-1, pmk-1, ins-7 and ilys3 immune genes of C. elegans were examined with live bacterial and isolated lipid moiety infection and the expression was found to be highly specific. Overall, the present study revealed that PAO1 modified its 2 and 2' amide linked fatty acid chain in the lipid A of PAO1 LPS during the exposed host condition.
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Registered trials
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