ArticleInfection and immunity1998
Burkholderia cepacia produces a hemolysin that is capable of inducing apoptosis and degranulation of mammalian phagocytes.
Article in Infection and immunity, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 104 citations in OpenAlex.
- Secretion systems shaping host-pathogen interactions in Burkholderia species.Applied microbiology and biotechnology · 2026Review
- A flagella-dependentmBio · 2025Article
- Biocontrol of biofilm forming Burkholderia cepacia using a quorum quenching crude lactonase enzyme extract from a marine Chromohalobacter sp. strain D23.Archives of microbiology · 2023Article
- Secretome analysis of an environmental isolate Enterobacter sp. S-33 identifies proteins related to pathogenicity.Archives of microbiology · 2022Article
- Article
- Staphylococcus aureus Potentiates the Hemolytic Activity of Burkholderia cepacia Complex (Bcc) Bacteria.Current microbiology · 2021Article
- Outer membrane vesicles produced byVirulence · 2020Article
- Review
- Characterization of Burkholderia pseudomallei protein BPSL1375 validates the Putative hemolytic activity of the COG3176 N-Acyltransferase family.BMC microbiology · 2015Article
- Residence in biofilms allows Burkholderia cepacia complex (Bcc) bacteria to evade the antimicrobial activities of neutrophil-like dHL60 cells.Pathogens and disease · 2015Article
- Article
- Active and secreted IgA-coated bacterial fractions from the human gut reveal an under-represented microbiota core.Scientific reports · 2013Article
- A Burkholderia cepacia complex non-ribosomal peptide-synthesized toxin is hemolytic and required for full virulence.Virulence · 2012Article
- Article
- Exploring the metabolic network of the epidemic pathogen Burkholderia cenocepacia J2315 via genome-scale reconstruction.BMC systems biology · 2011Article
- The type II secretion system is essential for erythrocyte lysis and gut colonization by the leech digestive tract symbiont Aeromonas veronii.Applied and environmental microbiology · 2011Article
- Profiling of Burkholderia cepacia secretome at mid-logarithmic and early-stationary phases of growth.PloS one · 2011Article
- Burkholderia cepacia Complex: Emerging Multihost Pathogens Equipped with a Wide Range of Virulence Factors and Determinants.International journal of microbiology · 2011Article
- Identification of potential therapeutic targets for Burkholderia cenocepacia by comparative transcriptomics.PloS one · 2010Article
- Neutrophil apoptosis and the resolution of infection.Immunologic research · 2009Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Burkholderia cepacia is an opportunistic pathogen that has become a major threat to individuals with cystic fibrosis (CF). In approximately 20% of patients, pulmonary colonization with B. cepacia leads to cepacia syndrome, a fatal fulminating pneumonia sometimes associated with septicemia. It has been reported that culture filtrates of clinically derived strains of B. cepacia are hemolytic. In this study, we have characterized a factor which contributes to this hemolytic activity and is secreted from B. cepacia J2315, a representative of the virulent and highly transmissible strain belonging to the recently described genomovar III grouping. Biochemical data from the described purification method for this hemolysin allows us to hypothesize that the toxin is a lipopeptide. As demonstrated for other lipopeptide toxins, the hemolysin from B. cepacia was surface active and lowered the surface tension of high-pressure liquid chromatography-grade water from 72.96 to 29.8 mN m(-1). Similar to reports for other pore-forming cytotoxins, low concentrations of the hemolysin were able to induce nucleosomal degradation consistent with apoptosis in human neutrophils and the mouse-derived macrophage-type cell line J774.2. Exposure of human neutrophils to higher concentrations of toxin resulted in increased activities of the neutrophil degranulation markers cathepsin G and elastase. Based on the results obtained in this study, we suggest a role that allows B. cepacia to thwart the immune response and a model of the events that may contribute to the severe inflammatory response in the lungs of CF patients.
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