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Highly purified lipoteichoic acid induced pro-inflammatory signalling in primary culture of rat microglia through Toll-like receptor 2: selective potentiation of nitric oxide production by muramyl dipeptide.
J Neurochem 2006; 99(2):596-607JN

Abstract

In contrast to the role of lipopolysaccharide from Gram-negative bacteria, the role of Gram-positive bacterial components in inducing inflammation in the CNS remains controversial. We studied the potency of highly purified lipoteichoic acid and muramyl dipeptide isolated from Staphylococcus aureus to activate primary cultures of rat microglia. Exposure of pure microglial cultures to lipoteichoic acid triggered a significant time- and dose-dependent production of pro-inflammatory cytokines (tumour-necrosis factor-alpha, interleukin-1beta, interleukin-6) and nitric oxide. Muramyl dipeptide strongly and selectively potentiated lipoteichoic acid-induced inducible nitric oxide synthase expression and nitric oxide production. However, it did not have any significant influence on the production of pro-inflammatory cytokines. As bacterial components are recognised by the innate immunity through Toll-like receptors (TLRs) we showed that lipoteichoic acid was recognised in microglia by the TLR2 and lipopolysaccharide by the TLR4, as cells isolated from mice lacking TLR2 or TLR4 did not produce pro-inflammatory cytokines and nitric oxide upon lipoteichoic acid or lipopolysaccharide stimulation, respectively. Lipoteichoic acid-induced glia activation was mediated by p38 and ERK1/2 MAP kinases, as pretreatment with inhibitor of p38 or ERK1/2 decreased lipoteichoic acid-induced cytokine release, iNOS mRNA expression and nitric oxide production. The observed pro-inflammatory response induced by lipoteichoic acid-activated microglia could play a major role in the inflammatory response of CNS induced by Gram-positive bacteria.

Authors+Show Affiliations

European Centre for the Validation of Alternative Methods, ECVAM, European Commission Joint Research Centre, Ispra, VA, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16879708

Citation

Kinsner, Agnieszka, et al. "Highly Purified Lipoteichoic Acid Induced Pro-inflammatory Signalling in Primary Culture of Rat Microglia Through Toll-like Receptor 2: Selective Potentiation of Nitric Oxide Production By Muramyl Dipeptide." Journal of Neurochemistry, vol. 99, no. 2, 2006, pp. 596-607.
Kinsner A, Boveri M, Hareng L, et al. Highly purified lipoteichoic acid induced pro-inflammatory signalling in primary culture of rat microglia through Toll-like receptor 2: selective potentiation of nitric oxide production by muramyl dipeptide. J Neurochem. 2006;99(2):596-607.
Kinsner, A., Boveri, M., Hareng, L., Brown, G. C., Coecke, S., Hartung, T., & Bal-Price, A. (2006). Highly purified lipoteichoic acid induced pro-inflammatory signalling in primary culture of rat microglia through Toll-like receptor 2: selective potentiation of nitric oxide production by muramyl dipeptide. Journal of Neurochemistry, 99(2), pp. 596-607.
Kinsner A, et al. Highly Purified Lipoteichoic Acid Induced Pro-inflammatory Signalling in Primary Culture of Rat Microglia Through Toll-like Receptor 2: Selective Potentiation of Nitric Oxide Production By Muramyl Dipeptide. J Neurochem. 2006;99(2):596-607. PubMed PMID: 16879708.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Highly purified lipoteichoic acid induced pro-inflammatory signalling in primary culture of rat microglia through Toll-like receptor 2: selective potentiation of nitric oxide production by muramyl dipeptide. AU - Kinsner,Agnieszka, AU - Boveri,Monica, AU - Hareng,Lars, AU - Brown,Guy C, AU - Coecke,Sandra, AU - Hartung,Thomas, AU - Bal-Price,Anna, Y1 - 2006/07/31/ PY - 2006/8/2/pubmed PY - 2007/1/9/medline PY - 2006/8/2/entrez SP - 596 EP - 607 JF - Journal of neurochemistry JO - J. Neurochem. VL - 99 IS - 2 N2 - In contrast to the role of lipopolysaccharide from Gram-negative bacteria, the role of Gram-positive bacterial components in inducing inflammation in the CNS remains controversial. We studied the potency of highly purified lipoteichoic acid and muramyl dipeptide isolated from Staphylococcus aureus to activate primary cultures of rat microglia. Exposure of pure microglial cultures to lipoteichoic acid triggered a significant time- and dose-dependent production of pro-inflammatory cytokines (tumour-necrosis factor-alpha, interleukin-1beta, interleukin-6) and nitric oxide. Muramyl dipeptide strongly and selectively potentiated lipoteichoic acid-induced inducible nitric oxide synthase expression and nitric oxide production. However, it did not have any significant influence on the production of pro-inflammatory cytokines. As bacterial components are recognised by the innate immunity through Toll-like receptors (TLRs) we showed that lipoteichoic acid was recognised in microglia by the TLR2 and lipopolysaccharide by the TLR4, as cells isolated from mice lacking TLR2 or TLR4 did not produce pro-inflammatory cytokines and nitric oxide upon lipoteichoic acid or lipopolysaccharide stimulation, respectively. Lipoteichoic acid-induced glia activation was mediated by p38 and ERK1/2 MAP kinases, as pretreatment with inhibitor of p38 or ERK1/2 decreased lipoteichoic acid-induced cytokine release, iNOS mRNA expression and nitric oxide production. The observed pro-inflammatory response induced by lipoteichoic acid-activated microglia could play a major role in the inflammatory response of CNS induced by Gram-positive bacteria. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/16879708/Highly_purified_lipoteichoic_acid_induced_pro_inflammatory_signalling_in_primary_culture_of_rat_microglia_through_Toll_like_receptor_2:_selective_potentiation_of_nitric_oxide_production_by_muramyl_dipeptide_ L2 - https://doi.org/10.1111/j.1471-4159.2006.04085.x DB - PRIME DP - Unbound Medicine ER -