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Signal transduction pathways of nitric oxide release in primary microglial culture challenged with gram-positive bacterial constituent, lipoteichoic acid.

Abstract

Between one-third and one-half of all cases of sepsis are known to be caused by gram-positive microorganisms through the cell wall component, e.g. lipoteichoic acid (LTA). Gram-positive bacteria are also known to induce encephalomyelitis and meningeal inflammation, and enhance the production of nitric oxide (NO) via expression of inducible nitric oxide synthase (iNOS) in murine tissue macrophages. It remains to be explored if LTA could activate microglia considered to be resident brain macrophages. We report here that LTA derived from gram-positive bacteria (Staphylococcus aureus) significantly induces NO release and iNOS expression in primary microglia. LTA-induced NO accumulation was detected at 2 h in microglial culture and was significantly attenuated by pretreatment with anti-CD14, complement receptor type 3 (CR3) or scavenger receptor (SR) antibodies. LTA activated mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase, p38 MAPK or c-Jun N-terminal kinase in cultured microglia. LTA-elicited microglial NO production was also drastically suppressed by SB203580 (p38 MAPK inhibitor) or pyrrolidine dithiocarbamate (an inhibitor of nuclear factor kappaB), indicating that p38 MAPK and nuclear factor kappaB were involved in microglial NO release after LTA challenge. These results suggest that gram-positive bacterial product such as LTA can activate microglia to release NO via the signal transduction pathway involving multiple LTA receptors (e.g. CD14, CR3 or SR), p38 MAPK and nuclear factor kappaB. The in vivo study further confirmed that administered intracerebrally LTA induced considerable noticeable iNOS, phospho-IkappaB and phospho-p38 MAPK expression in microglia/macrophages.

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  • Authors+Show Affiliations

    ,

    Department of Surgery, College of Medicine, National Taiwan University, 1, Section 1, Jen-Ai Road, Taipei 100, Taiwan.

    , , , , ,

    Source

    Neuroscience 133:2 2005 pg 423-36

    MeSH

    Animals
    Antibodies
    Blotting, Western
    Carbidopa
    Cells, Cultured
    Dose-Response Relationship, Drug
    Drug Combinations
    Eye Proteins
    Fluorescent Antibody Technique
    Gene Expression Regulation
    I-kappa B Proteins
    Indoles
    Lectins
    Levodopa
    Lipopolysaccharide Receptors
    Lipopolysaccharides
    Microglia
    Nerve Tissue Proteins
    Nitric Oxide
    Nitric Oxide Synthase
    Nitric Oxide Synthase Type II
    Nitrites
    Rats
    Rats, Wistar
    Signal Transduction
    Teichoic Acids
    Time Factors
    gamma-Synuclein
    p38 Mitogen-Activated Protein Kinases

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    15878805

    Citation

    Chien, H F., et al. "Signal Transduction Pathways of Nitric Oxide Release in Primary Microglial Culture Challenged With Gram-positive Bacterial Constituent, Lipoteichoic Acid." Neuroscience, vol. 133, no. 2, 2005, pp. 423-36.
    Chien HF, Yeh KY, Jiang-Shieh YF, et al. Signal transduction pathways of nitric oxide release in primary microglial culture challenged with gram-positive bacterial constituent, lipoteichoic acid. Neuroscience. 2005;133(2):423-36.
    Chien, H. F., Yeh, K. Y., Jiang-Shieh, Y. F., Wei, I. H., Chang, C. Y., Chang, M. L., & Wu, C. H. (2005). Signal transduction pathways of nitric oxide release in primary microglial culture challenged with gram-positive bacterial constituent, lipoteichoic acid. Neuroscience, 133(2), pp. 423-36.
    Chien HF, et al. Signal Transduction Pathways of Nitric Oxide Release in Primary Microglial Culture Challenged With Gram-positive Bacterial Constituent, Lipoteichoic Acid. Neuroscience. 2005;133(2):423-36. PubMed PMID: 15878805.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Signal transduction pathways of nitric oxide release in primary microglial culture challenged with gram-positive bacterial constituent, lipoteichoic acid. AU - Chien,H F, AU - Yeh,K Y, AU - Jiang-Shieh,Y F, AU - Wei,I H, AU - Chang,C Y, AU - Chang,M L, AU - Wu,C H, PY - 2004/05/24/received PY - 2004/08/25/revised PY - 2004/09/17/accepted PY - 2005/5/10/pubmed PY - 2005/9/1/medline PY - 2005/5/10/entrez SP - 423 EP - 36 JF - Neuroscience JO - Neuroscience VL - 133 IS - 2 N2 - Between one-third and one-half of all cases of sepsis are known to be caused by gram-positive microorganisms through the cell wall component, e.g. lipoteichoic acid (LTA). Gram-positive bacteria are also known to induce encephalomyelitis and meningeal inflammation, and enhance the production of nitric oxide (NO) via expression of inducible nitric oxide synthase (iNOS) in murine tissue macrophages. It remains to be explored if LTA could activate microglia considered to be resident brain macrophages. We report here that LTA derived from gram-positive bacteria (Staphylococcus aureus) significantly induces NO release and iNOS expression in primary microglia. LTA-induced NO accumulation was detected at 2 h in microglial culture and was significantly attenuated by pretreatment with anti-CD14, complement receptor type 3 (CR3) or scavenger receptor (SR) antibodies. LTA activated mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase, p38 MAPK or c-Jun N-terminal kinase in cultured microglia. LTA-elicited microglial NO production was also drastically suppressed by SB203580 (p38 MAPK inhibitor) or pyrrolidine dithiocarbamate (an inhibitor of nuclear factor kappaB), indicating that p38 MAPK and nuclear factor kappaB were involved in microglial NO release after LTA challenge. These results suggest that gram-positive bacterial product such as LTA can activate microglia to release NO via the signal transduction pathway involving multiple LTA receptors (e.g. CD14, CR3 or SR), p38 MAPK and nuclear factor kappaB. The in vivo study further confirmed that administered intracerebrally LTA induced considerable noticeable iNOS, phospho-IkappaB and phospho-p38 MAPK expression in microglia/macrophages. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/15878805/Signal_transduction_pathways_of_nitric_oxide_release_in_primary_microglial_culture_challenged_with_gram_positive_bacterial_constituent_lipoteichoic_acid_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(04)00857-7 DB - PRIME DP - Unbound Medicine ER -