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Lipid A Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia pseudomallei.
Infect Immun. 2018 10; 86(10)II

Abstract

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.

Authors+Show Affiliations

Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA mhnorris@ufl.edu.Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute, University of Florida, Gainesville, Florida, USA.Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute, University of Florida, Gainesville, Florida, USA.Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30037795

Citation

Norris, Michael H., et al. "Lipid a Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia Pseudomallei." Infection and Immunity, vol. 86, no. 10, 2018.
Norris MH, Somprasong N, Schweizer HP, et al. Lipid A Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia pseudomallei. Infect Immun. 2018;86(10).
Norris, M. H., Somprasong, N., Schweizer, H. P., & Tuanyok, A. (2018). Lipid A Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia pseudomallei. Infection and Immunity, 86(10). https://doi.org/10.1128/IAI.00360-18
Norris MH, et al. Lipid a Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia Pseudomallei. Infect Immun. 2018;86(10) PubMed PMID: 30037795.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lipid A Remodeling Is a Pathoadaptive Mechanism That Impacts Lipopolysaccharide Recognition and Intracellular Survival of Burkholderia pseudomallei. AU - Norris,Michael H, AU - Somprasong,Nawarat, AU - Schweizer,Herbert P, AU - Tuanyok,Apichai, Y1 - 2018/09/21/ PY - 2018/05/10/received PY - 2018/07/13/accepted PY - 2018/7/25/pubmed PY - 2019/4/17/medline PY - 2018/7/25/entrez KW - Burkholderia pseudomallei KW - inflammasome KW - intracellular pathogen KW - lipid A KW - lipopolysaccharide JF - Infection and immunity JO - Infect Immun VL - 86 IS - 10 N2 - 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. SN - 1098-5522 UR - https://www.unboundmedicine.com/medline/citation/30037795/Lipid_A_Remodeling_Is_a_Pathoadaptive_Mechanism_That_Impacts_Lipopolysaccharide_Recognition_and_Intracellular_Survival_of_Burkholderia_pseudomallei_ L2 - http://iai.asm.org/lookup/pmidlookup?view=long&pmid=30037795 DB - PRIME DP - Unbound Medicine ER -