Document Detail


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.
MedLine Citation:
PMID:  12452837     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
M P Jagger; Z Huo; P G Riches
Related Documents :
12135807 - Initial responses to endotoxins and gram-negative bacteria.
11090937 - Endotoxins, asthma, and allergic immune responses.
20939997 - Ephedrannin a and b from roots of ephedra sinica inhibit lipopolysaccharide-induced inf...
18622687 - Modulation of lps-induced pulmonary neutrophil infiltration and cytokine production by ...
15325797 - Nicotinic environment affects the differentiation and functional maturation of monocyte...
11509677 - The role of macrophages in glomerulonephritis.
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental immunology     Volume:  130     ISSN:  0009-9104     ISO Abbreviation:  Clin. Exp. Immunol.     Publication Date:  2002 Dec 
Date Detail:
Created Date:  2002-11-27     Completed Date:  2003-03-03     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0057202     Medline TA:  Clin Exp Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  467-74     Citation Subset:  IM    
Affiliation:
Department of Biochemistry and Immunology St George's Hospital Medical School, London, UK.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Bacterial Capsules / pharmacology*
Blood Bactericidal Activity*
Dose-Response Relationship, Drug
Enzyme-Linked Immunosorbent Assay / methods
Humans
Interleukin-6 / biosynthesis
Lipopolysaccharides / pharmacology
Microspheres
Monokines / biosynthesis*
Shock, Septic / immunology*,  microbiology
Statistics, Nonparametric
Streptococcus pneumoniae / immunology*
Tumor Necrosis Factor-alpha / biosynthesis
Chemical
Reg. No./Substance:
0/Interleukin-6; 0/Lipopolysaccharides; 0/Monokines; 0/Tumor Necrosis Factor-alpha; 0/pneumococcal polysaccharide, type 14
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Murine glomerular mesangial cell uptake of apoptotic cells is inefficient and involves serum-mediate...
Next Document:  Transcriptional regulation of the IL-5 gene in peripheral T cells of asthmatic patients.