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Norris MH, Somprasong N, Schweizer HP, Tuanyok A
Lipid A Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia pseudomallei
Infection and Immunity 86(10) (2018)
e00360-18
R-3HOMyr-(1-3)-+
|
?%b-L-Arap4N-(1--P--1)--+ |
| |
Lau-(1-3)-R-3HOMyr-(1-2)-+ | |
| | |
S-2HOMyr-(1-3)-R-3HOMyr-(1-3)-b-D-GlcpN-(1-6)-a-D-GlcpN
| |
?%b-L-Arap4N-(1--P--4)--+ |
|
R-3HOMyr-(1-2)-+ |
Show graphically |
Salmonella enterica sv. Typhimurium
(later renamed to: Salmonella enterica ssp. enterica sv. Typhimurium)
(NCBI TaxID 90371,
species name lookup)
Taxonomic group: bacteria / Proteobacteria
(Phylum: Proteobacteria)
Associated disease: infection due to Salmonella enterica [ICD11:
XN5VC 
]
NCBI PubMed ID: 30037795Publication DOI: 10.1128/IAI.00360-18Journal NLM ID: 0246127Publisher: American Society for Microbiology
Correspondence: mhnorris

ufl.edu
Institutions: Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA, Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute, University of Florida, Gainesville, Florida, USA
Burkholderia pseudomallei causes the severe disease melioidosis. The bacterium subverts the host immune system and replicates inside cells, and host mortality results primarily from sepsis-related complications. Lipopolysaccharide (LPS) is a major virulence factor and mediator of sepsis that many pathogens capable of intracellular growth modify to reduce their immunological 'footprint.' The binding strength of B. pseudomallei LPS for human LPS binding protein (hLBP) was measured using surface plasmon resonance. The structures of lipid A isolated from B. pseudomallei under different temperatures were analyzed by matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), and the gene expression of two lipid A remodeling genes, lpxO and pagL, was investigated. The LPS was characterized for its ability to trigger tumor necrosis factor alpha (TNF-α) release and to activate caspase-11-triggered pyroptosis by introduction of LPS into the cytosol. Lipid A from long-term chronic-infection isolates was isolated and characterized by MALDI-TOF MS and also by the ability to trigger caspase-11-mediated cell death. Lipid A from B. pseudomallei 1026b lpxO and pagL mutants were characterized by positive- and negative-mode MALDI-TOF MS to ultimately identify their role in lipid A structural modifications. Replication of lpxO and pagL mutants and their complements within macrophages showed that lipid A remodeling can effect growth in host cells and activation of caspase-11-mediated cytotoxicity.
Lipopolysaccharide, lipid A, Burkholderia pseudomallei, inflammasome, intracellular pathogen
Structure type: oligomer
Location inside paper: fig.1A, S. enterica lipid A
Compound class: lipid A
Contained glycoepitopes: IEDB_137340,IEDB_141807,IEDB_151531,IEDB_534864
Methods: DNA techniques, MALDI-TOF MS, cytokines tumor necrosis factor alpha (TNF-a) assay, SPR, cytotoxicity assay, inflammasome activation assays
Related record ID(s): 12955
NCBI Taxonomy refs (TaxIDs): 90371
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Norris MH, Somprasong N, Schweizer HP, Tuanyok A
Lipid A Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia pseudomallei
Infection and Immunity 86(10) (2018)
e00360-18
R-3HOMyr-(1-3)-+
|
?%b-L-Arap4N-(1--P--1)--+ |
| |
?%b-L-Arap4N-(1--P--4)--+ | |
| | |
Myr-(1-3)-R-3HOPam-(1-2)-b-D-GlcpN-(1-6)-a-D-GlcpN
| |
R-3HOMyr-(1-3)-+ |
|
R-3HOPam-(1-2)-+ |
Show graphically |
Burkholderia pseudomallei
(NCBI TaxID 28450,
species name lookup)
Taxonomic group: bacteria / Proteobacteria
(Phylum: Proteobacteria)
Associated disease: melioidosis [ICD11:
1C42 
, ICD11:
XN3LD 
];
infection due to Burkholderia pseudomallei [ICD11:
XN3LD 
]
NCBI PubMed ID: 30037795Publication DOI: 10.1128/IAI.00360-18Journal NLM ID: 0246127Publisher: American Society for Microbiology
Correspondence: mhnorris

ufl.edu
Institutions: Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA, Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute, University of Florida, Gainesville, Florida, USA
Burkholderia pseudomallei causes the severe disease melioidosis. The bacterium subverts the host immune system and replicates inside cells, and host mortality results primarily from sepsis-related complications. Lipopolysaccharide (LPS) is a major virulence factor and mediator of sepsis that many pathogens capable of intracellular growth modify to reduce their immunological 'footprint.' The binding strength of B. pseudomallei LPS for human LPS binding protein (hLBP) was measured using surface plasmon resonance. The structures of lipid A isolated from B. pseudomallei under different temperatures were analyzed by matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), and the gene expression of two lipid A remodeling genes, lpxO and pagL, was investigated. The LPS was characterized for its ability to trigger tumor necrosis factor alpha (TNF-α) release and to activate caspase-11-triggered pyroptosis by introduction of LPS into the cytosol. Lipid A from long-term chronic-infection isolates was isolated and characterized by MALDI-TOF MS and also by the ability to trigger caspase-11-mediated cell death. Lipid A from B. pseudomallei 1026b lpxO and pagL mutants were characterized by positive- and negative-mode MALDI-TOF MS to ultimately identify their role in lipid A structural modifications. Replication of lpxO and pagL mutants and their complements within macrophages showed that lipid A remodeling can effect growth in host cells and activation of caspase-11-mediated cytotoxicity.
Lipopolysaccharide, lipid A, Burkholderia pseudomallei, inflammasome, intracellular pathogen
Structure type: oligomer
Location inside paper: fig.1B, B. pseudomallei lipid A
Compound class: lipid A
Contained glycoepitopes: IEDB_137340,IEDB_141807,IEDB_151531,IEDB_176772
Methods: DNA techniques, MALDI-TOF MS, cytokines tumor necrosis factor alpha (TNF-a) assay, SPR, cytotoxicity assay, inflammasome activation assays
Related record ID(s): 12750
NCBI Taxonomy refs (TaxIDs): 28450
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