Taxonomic group: bacteria / Proteobacteria
(Phylum: Proteobacteria)
Host organism: Homo sapiens
Associated disease: cystic fibrosis (CF) [ICD11:
CA25 
];
infection due to Pseudomonas aeruginosa [ICD11:
XN5L6 ]
NCBI PubMed ID: 20593270Publication DOI: 10.1007/978-90-481-9078-2_11Publisher: Springer.
Editors: Wang X, Quinn PJ
Correspondence: rkernst
umaryland.edu
Institutions: Department of Microbial Pathogenesis, School of Dentistry, University of Maryland - Baltimore, 650 W. Baltimore Street - 8 South, Baltimore, MD, 21201, USA
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.
Lipopolysaccharide, Pseudomonas aeruginosa, lipid A, inflammation, cystic fibrosis, innate immunity, antibiotic resistance, chronic infection
Structure type: oligomer ; 1617
Location inside paper: p.248, fig.11.3B, p.246, fig.11.2D
Compound class: lipid A
Contained glycoepitopes: IEDB_135394,IEDB_135515,IEDB_141807,IEDB_151531,IEDB_534864
Enzymes that release or process the structure: HtrB1 (lauryltransferase), LpxO (the lipid A-specific hydroxylase)
Comments, role: review; lipid A from acute clinical infection or non-CF (cystic fibrosis) bronchiectasis isolates.
Related record ID(s): 25356, 31943, 31945, 31946, 31947
NCBI Taxonomy refs (TaxIDs): 287
Show glycosyltransferases
There is only one chemically distinct structure:
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