ArticlePloS one2013
Survey of innate immune responses to Burkholderia pseudomallei in human blood identifies a central role for lipopolysaccharide.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- Dysfunctional host cellular immune responses are associated with mortality in melioidosis.Emerging microbes & infections · 2024Article
- Flagellin-modulated inflammasome pathways characterize the human alveolar macrophage response toInfection and immunity · 2024Article
- The Arabinose 5-Phosphate Isomerase KdsD Is Required for Virulence in Burkholderia pseudomallei.Journal of bacteriology · 2023Article
- Melioidosis Patient Survival Correlates With Strong IFN-γ Secreting T Cell Responses Against Hcp1 and TssM.Frontiers in immunology · 2021Article
- A DUF4148 family protein produced inside RAW264.7 cells is a critical Burkholderia pseudomallei virulence factor.Virulence · 2020Article
- Lactoferrin is a dynamic protein in human melioidosis and is a TLR4-dependent driver of TNF-α release in Burkholderia thailandensis infection in vitro.PLoS neglected tropical diseases · 2020Article
- Longitudinal profiling of plasma cytokines in melioidosis and their association with mortality: a prospective cohort study.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2020Article
- Lipopolysaccharide Recognition in the Crossroads of TLR4 and Caspase-4/11 Mediated Inflammatory Pathways.Frontiers in immunology · 2020Review
- Like Cures Like: Pharmacological Activity of Anti-Inflammatory Lipopolysaccharides From Gut Microbiome.Frontiers in pharmacology · 2020Review
- Flagellin-independent effects of a Toll-like receptor 5 polymorphism in the inflammatory response to Burkholderia pseudomallei.PLoS neglected tropical diseases · 2019Article
- Implications of environmental and pathogen-specific determinants on clinical presentations and disease outcome in melioidosis patients.PLoS neglected tropical diseases · 2019Article
- Effects and Mechanism of Nano-Copper Exposure on Hepatic Cytochrome P450 Enzymes in Rats.International journal of molecular sciences · 2018Article
- Comprehensive analysis of clinical Burkholderia pseudomallei isolates demonstrates conservation of unique lipid A structure and TLR4-dependent innate immune activation.PLoS neglected tropical diseases · 2018Article
- Article
- Deciphering minimal antigenic epitopes associated with Burkholderia pseudomallei and Burkholderia mallei lipopolysaccharide O-antigens.Nature communications · 2017Article
- Current challenges in the management of sepsis in ICUs in resource-poor settings and suggestions for the future.Intensive care medicine · 2017Review
- Structural diversity of Burkholderia pseudomallei lipopolysaccharides affects innate immune signaling.PLoS neglected tropical diseases · 2017Article
- Interleukin 10 inhibits pro-inflammatory cytokine responses and killing of Burkholderia pseudomallei.Scientific reports · 2017Article
- TLR4 genetic variation is associated with inflammatory responses in Gram-positive sepsis.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2017Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
B. pseudomallei is a gram-negative bacterium that causes the tropical infection melioidosis. In northeast Thailand, mortality from melioidosis approaches 40%. As exemplified by the lipopolysaccharide-Toll-like receptor 4 interaction, innate immune responses to invading bacteria are precipitated by activation of host pathogen recognition receptors by pathogen associated molecular patterns. Human melioidosis is characterized by up-regulation of pathogen recognition receptors and pro-inflammatory cytokine release. In contrast to many gram-negative pathogens, however, the lipopolysaccharide of B. pseudomallei is considered only weakly inflammatory. We conducted a study in 300 healthy Thai subjects to investigate the ex vivo human blood response to various bacterial pathogen associated molecular patterns, including lipopolysaccharide from several bacteria, and to two heat-killed B. pseudomallei isolates. We measured cytokine levels after stimulation of fresh whole blood with a panel of stimuli. We found that age, sex, and white blood cell count modulate the innate immune response to B. pseudomallei. We further observed that, in comparison to other stimuli, the innate immune response to B. pseudomallei is most highly correlated with the response to lipopolysaccharide. The magnitude of cytokine responses induced by B. pseudomallei lipopolysaccharide was significantly greater than those induced by lipopolysaccharide from Escherichia coli and comparable to many responses induced by lipopolysaccharide from Salmonella minnesota despite lower amounts of lipid A in the B. pseudomallei lipopolysaccharide preparation. In human monocytes stimulated with B. pseudomallei, addition of polymyxin B or a TLR4/MD-2 neutralizing antibody inhibited the majority of TNF-α production. Challenging existing views, our data indicate that the innate immune response to B. pseudomallei in human blood is largely driven by lipopolysaccharide, and that the response to B. pseudomallei lipopolysaccharide in blood is greater than the response to other lipopolysaccharide expressing isolates. Our findings suggest that B. pseudomallei lipopolysaccharide may play a central role in stimulating the host response in melioidosis.
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Registered trials
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