ArticleBMC immunology2011
Distinct roles for nitric oxide in resistant C57BL/6 and susceptible BALB/c mice to control Burkholderia pseudomallei infection.
Article in BMC immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Burkholderia pseudomallei triggers canonical inflammasome activation in a human primary macrophage-based infection model.PLoS neglected tropical diseases · 2020Article
- Burkholderia pseudomallei modulates host iron homeostasis to facilitate iron availability and intracellular survival.PLoS neglected tropical diseases · 2018Article
- Relative susceptibility of airway organisms to antimicrobial effects of nitric oxide.International forum of allergy & rhinology · 2017Article
- Article
- Mapping epigenetic changes to the host cell genome induced by Burkholderia pseudomallei reveals pathogen-specific and pathogen-generic signatures of infection.Scientific reports · 2016Article
- The art of persistence-the secrets to Burkholderia chronic infections.Pathogens and disease · 2016Review
- The mouse antibody heavy chain repertoire is germline-focused and highly variable between inbred strains.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Article
- Nitric oxide suppresses LPS-induced inflammation in a mouse asthma model by attenuating the interaction of IKK and Hsp90.Experimental biology and medicine (Maywood, N.J.) · 2015Article
- Interaction of Interferon gamma-induced reactive oxygen species with ceftazidime leads to synergistic killing of intracellular Burkholderia pseudomallei.Antimicrobial agents and chemotherapy · 2014Article
- Neutrophil elastase causes tissue damage that decreases host tolerance to lung infection with burkholderia species.PLoS pathogens · 2014Article
- Sterile-α- and armadillo motif-containing protein inhibits the TRIF-dependent downregulation of signal regulatory protein α to interfere with intracellular bacterial elimination in Burkholderia pseudomallei-infected mouse macrophages.Infection and immunity · 2013Article
- Increased resistance to Staphylococcus aureus endophthalmitis in BALB/c mice: Fas ligand is required for resolution of inflammation but not for bacterial clearance.Infection and immunity · 2013Article
- Development of Burkholderia mallei and pseudomallei vaccines.Frontiers in cellular and infection microbiology · 2013Review
- Nitric oxide-dependent killing of aerobic, anaerobic and persistent Burkholderia pseudomallei.Nitric oxide : biology and chemistry · 2012Article
- Defense Mechanisms of Hepatocytes Against Burkholderia pseudomallei.Frontiers in microbiology · 2011Article
- Development of vaccines against burkholderia pseudomallei.Frontiers in microbiology · 2011Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBurkholderia pseudomallei is the causative agent of melioidosis, an emerging bacterial infectious disease in tropical and subtropical areas. We recently showed that NADPH oxidase but not nitric oxide (NO) contributes to resistance in innately resistant C57BL/6 mice in a B. pseudomallei respiratory infection model. However, the function of NO for resistance was shown to differ among distinct strains of mice and proved also to be stage dependent in various infection models. The present study therefore aimed to examine the role of NO in a systemic infection model of melioidosis and to test whether the function of NO differs among innately resistant C57BL/6 and susceptible BALB/c mice after B. pseudomallei infection.
resultsC57BL/6 iNOS-/- mice that were intravenously infected with B. pseudomallei survived several weeks, whereas most of the wild type animals succumbed during this period. The bacterial burden in liver and spleen was significantly higher in wild type animals compared to iNOS-/- mice 13 days after challenge. In contrast, BALB/c mice that were treated with amminoguanidine to inhibit NO expression in vivo showed significantly enhanced mortality rates and higher bacterial loads in liver and spleen compared to control animals. The bactericidal function of IFN-γ stimulated C57BL/6 iNOS-/- macrophages were not altered after B. pseudomallei infection, but BALB/c macrophages exhibited reduced killing activity against the pathogen when NO was inhibited.
conclusionOur present data indicate a dual role of NO among resistant and susceptible mouse strains after B. pseudomallei infection. NO mediated mechanisms are an essential component to control the infection in susceptible BALB/c mice. In contrast, NO production in B. pseudomallei infected C57BL/6 mice rather harmed the host likely due to its detrimental effects.
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