ArticleClinical and experimental immunology2000
Kinetic studies of the production of nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) in macrophages stimulated with Burkholderia pseudomallei endotoxin.
Article in Clinical and experimental immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Melioidosis vaccines: a systematic review and appraisal of the potential to exploit biodefense vaccines for public health purposes.PLoS neglected tropical diseases · 2012Pooled it
- Nitric Oxide Tunes Secreted Metabolite Bioactivity.Molecular microbiology · 2026Article
- Intracellular behavior ofFrontiers in cellular and infection microbiology · 2023Article
- Involvement of L-selectin expression in Burkholderia pseudomallei-infected monocytes invading the brain during murine melioidosis.Virulence · 2017Article
- Melioidosis: Clinical impact and public health threat in the tropics.PLoS neglected tropical diseases · 2017Review
- Characterization of in vitro phenotypes of Burkholderia pseudomallei and Burkholderia mallei strains potentially associated with persistent infection in mice.Archives of microbiology · 2017Article
- Burkholderia pseudomallei induces IL-23 production in primary human monocytes.Medical microbiology and immunology · 2016Article
- Characterization of Burkholderia pseudomallei Strains Using a Murine Intraperitoneal Infection Model and In Vitro Macrophage Assays.PloS one · 2015Article
- Delineating the importance of serum opsonins and the bacterial capsule in affecting the uptake and killing of Burkholderia pseudomallei by murine neutrophils and macrophages.PLoS neglected tropical diseases · 2014Article
- Survey of innate immune responses to Burkholderia pseudomallei in human blood identifies a central role for lipopolysaccharide.PloS one · 2013Article
- A naturally derived outer-membrane vesicle vaccine protects against lethal pulmonary Burkholderia pseudomallei infection.Vaccine · 2011Article
- Strategies for Intracellular Survival of Burkholderia pseudomallei.Frontiers in microbiology · 2011Article
- Genome wide transcriptome profiling of a murine acute melioidosis model reveals new insights into how Burkholderia pseudomallei overcomes host innate immunity.BMC genomics · 2010Article
- Differential susceptibility of inbred mouse strains to Burkholderia thailandensis aerosol infection.Microbial pathogenesis · 2010Article
- Innate immune responses of pulmonary epithelial cells to Burkholderia pseudomallei infection.PloS one · 2009Article
- Structural and biological diversity of lipopolysaccharides from Burkholderia pseudomallei and Burkholderia thailandensis.Clinical and vaccine immunology : CVI · 2009Article
- Burkholderia mallei cellular interactions in a respiratory cell model.Journal of medical microbiology · 2009Article
- Inactivation of [Fe-S] metalloproteins mediates nitric oxide-dependent killing of Burkholderia mallei.PloS one · 2008Article
- iNOS activity is critical for the clearance of Burkholderia mallei from infected RAW 264.7 murine macrophages.Cellular microbiology · 2008Article
- Fate of a Burkholderia pseudomallei lipopolysaccharide mutant in the mouse macrophage cell line RAW 264.7: possible role for the O-antigenic polysaccharide moiety of lipopolysaccharide in internalization and intracellular survival.Infection and immunity · 2007Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism by which Burkholderia pseudomallei survives in macrophages is not clearly understood. In this study, we demonstrated that the mouse macrophage cell line (RAW 264.7) treated with lipopolysaccharide (LPS) from B. pseudomallei (BP-LPS) produced significantly less NO and TNF-alpha compared with those stimulated with the LPS from Escherichia coli and Salmonella typhi. The time required for the BP-LPS to trigger substantial NO and TNF-alpha release was at least 30 min, compared with < 5 min for the E. coli-LPS. A time course study of inducible nitric oxide synthase (iNOS) protein expression also indicated that the time required for macrophages stimulated with the BP-LPS to up-regulate iNOS was longer. The longer time lag for the BP-LPS to activate macrophages was probably due to the delay in up-regulation of iNOS and TNF-alpha mRNA transcription. These results indirectly suggest that the delay of the mediators' production may be due to a reduced rate of signal transduction initiated by the interaction of BP-LPS with the macrophage cell surface. The use of MoAb to phosphorylated p38 in a Western blot analysis provided data compatible with the notion that the maximum level of phosphorylated p38 from the cells activated with BP-LPS was attained at a slower rate. These results suggest that the unique structure of BP-LPS exhibits a property which may interfere with macrophage cell activation.
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