ArticleClinical and experimental immunology2002
Inflammatory cytokine (interleukin 6 and tumour necrosis factor alpha) release in a human whole blood system in response to Streptococcus pneumoniae serotype 14 and its capsular polysaccharide.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- TLR-mediated inflammatory responses to Streptococcus pneumoniae are highly dependent on surface expression of bacterial lipoproteins.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
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- Mycobacterium tuberculosis Mannose-Capped Lipoarabinomannan Induces IL-10-Producing B Cells and Hinders CD4iScience · 2019Article
- Whole-blood incubation with the Neisseria meningitidis lpxL1 mutant induces less pro-inflammatory cytokines than the wild type, and IL-10 reduces the MyD88-dependent cytokines.Innate immunity · 2018Article
- Propofol increases morbidity and mortality in a rat model of sepsis.Critical care (London, England) · 2015Article
- Vesicle-independent extracellular release of a proinflammatory outer membrane lipoprotein in free-soluble form.BMC microbiology · 2008Article
- Influence of neutropenia on the course of serotype 8 pneumococcal pneumonia in mice.Infection and immunity · 2007Article
- Inflammatory response associated with pulmonary complications in non-HIV immunocompromised patients.Thorax · 2004Article
- Human immunodeficiency virus type 1 protease inhibitors block toll-like receptor 2 (TLR2)- and TLR4-Induced NF-kappaB activation.Antimicrobial agents and chemotherapy · 2004Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gram-positive bacteria, which lack lipopolysaccharide (LPS), produce a septic-shock-like condition, accompanied by release of pro-inflammatory cytokines. Various components of the bacteria may be responsible for this. We stimulated a whole blood system with heat-inactivated Streptococcus pneumoniae serotype 14 (S14) bacteria, with pneumococcal S14 capsular polysaccharide (PPS S14) and with PPS S14 coated on to latex beads, to compare interleukin 6 (IL-6) and tumour necrosis factor alpha (TNFalpha) production over a six hour period, to ascertain the contribution of PPS to the inflammatory response. This was compared with the response to LPS. After sonication of the bacteria, their PPS content was estimated by an enzyme-linked immunoabsorbent assay, to compare this with the concentration of free PPS needed to generate cytokine release. The whole bacteria elicited a much larger cytokine response than the equivalent amount of PPS alone, whereas the PPS-coated beads gave minimal response. The different cytokine responses to PPS and LPS suggest that there are differences in the receptors and/or signalling pathways for Gram-negative and Gram-positive bacteria. We conclude that the estimated amount of PPS in the bacteria is not enough to account for the large cytokine response we observed. Since PPS could not be shown to contribute significantly to cytokine induction, specific antibodies to PPS would not play any significant role in combating cytokine release associated with pneumococcal infection and possible septic shock. This needs to be considered in production of future vaccines.
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