Differences in Toll-like receptor expression and cytokine production after stimulation with heat-killed Gram-positive and Gram-negative bacteria
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Transcriptional Activation MeSH
- Cytokines biosynthesis MeSH
- Gram-Negative Bacteria genetics immunology MeSH
- Gram-Positive Bacteria genetics immunology MeSH
- Humans MeSH
- Monocytes immunology MeSH
- Immunity, Innate MeSH
- Gene Expression Regulation MeSH
- Signal Transduction immunology MeSH
- Toll-Like Receptor 2 biosynthesis genetics immunology MeSH
- Toll-Like Receptor 4 biosynthesis genetics immunology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cytokines MeSH
- Toll-Like Receptor 2 MeSH
- Toll-Like Receptor 4 MeSH
Innate immune surveillance in the blood is executed mostly by circulating monocytes, which recognise conserved bacterial molecules such as peptidoglycan and lipopolysaccharide. Toll-like receptors (TLR) play a central role in microbe-associated molecular pattern detection. Here, we compared the differences in TLR expression and cytokine production after stimulation of peripheral blood cells with heat-killed Gram-negative and Gram-positive human pathogens Neisseria meningitidis, Escherichia coli, Staphylococcus aureus and Streptococcus pneumoniae. We found that TLR2 expression is up-regulated on monocytes after stimulation with S. aureus, S. pneumoniae, E. coli and N. meningitidis. Moreover, TLR2 up-regulation was positively associated with increasing concentrations of Gram-positive bacteria, whereas higher concentrations of Gram-negative bacteria, especially E. coli, caused a milder TLR2 expression increase compared with low doses. Cytokines were produced in similar dose-dependent profiles regardless of the stimulatory pathogen; however, Gram-negative pathogens induced higher cytokine levels than Gram-positive ones at same concentrations. These results indicate that Gram-positive and Gram-negative bacteria differ in their dose-dependent patterns of induction of TLR2 and TLR4, but not in cytokine expression.
See more in PubMed
Pediatr Res. 2005 Oct;58(4):654-9 PubMed
J Immunol. 2000 Apr 1;164(7):3476-9 PubMed
Infect Immun. 2008 Sep;76(9):4183-9 PubMed
Clin Exp Immunol. 2004 May;136(2):312-9 PubMed
Infect Dis Clin North Am. 1999 Jun;13(2):299-312, vii PubMed
Arch Dis Child. 2002 Jan;86(1):44-6 PubMed
J Lipid Res. 2004 Apr;45(4):742-9 PubMed
J Immunol. 2004 Jul 15;173(2):1166-70 PubMed
Kidney Int. 1995 Nov;48(5):1469-76 PubMed
Clin Immunol. 2006 May;119(2):180-7 PubMed
Diagn Pathol. 2009 Apr 16;4:12 PubMed
Shock. 2003 Sep;20(3):224-9 PubMed
Cytokine. 2005 Dec 21;32(6):304-15 PubMed
J Exp Med. 2002 Mar 4;195(5):559-70 PubMed
Folia Microbiol (Praha). 2007;52(5):525-8 PubMed
Infect Immun. 2008 Feb;76(2):454-65 PubMed
