Bacillus anthracis lethal toxin attenuates lipoteichoic acid-induced maturation and activation of dendritic cells through a unique mechanism
Autor: | Young-Hee Ryu, Jihyun Yang, Min-Hee Cho, Cheol-Heui Yun, Sang Su Woo, Seung Hyun Han, Hee-Bok Oh, Gi-eun Rhie, Bong-Su Kim |
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Rok vydání: | 2009 |
Předmět: |
Lipopolysaccharides
Receptors Peptide Lipopolysaccharide MAP Kinase Signaling System Bacterial Toxins Immunology Bone Marrow Cells Receptors Cell Surface Microbiology Mice chemistry.chemical_compound Immune system Antigens CD MHC class I Biomarkers Tumor Animals Phosphorylation Receptor Molecular Biology CD86 Antigens Bacterial biology Histocompatibility Antigens Class I Microfilament Proteins Histocompatibility Antigens Class II Dendritic Cells biology.organism_classification Toll-Like Receptor 2 Bacillus anthracis Cell biology Teichoic Acids Gene Expression Regulation chemistry biology.protein Cytokines lipids (amino acids peptides and proteins) Lipoteichoic acid CD80 |
Zdroj: | Molecular Immunology. 46:3261-3268 |
ISSN: | 0161-5890 |
DOI: | 10.1016/j.molimm.2009.08.005 |
Popis: | Lethal toxin (LT), produced by the gram-positive bacterium Bacillus anthracis, was identified as a major etiologic agent causing anthrax due to its strong immunotoxicity. Gram-positive bacteria express lipoteichoic acid (LTA), which is considered as a counterpart to lipopolysaccharide (LPS) of gram-negative bacteria, but differs from LPS in the structure and function. Since dendritic cells (DCs) are essential for the appropriate initiation of immune response, we investigated the effect of LT on LTA-induced DC maturation using immature DCs prepared by differentiation of C57BL/6 mouse bone marrow cells. When immature DCs were matured with LTA in the presence of LT, the expression of representative markers for DC maturation such as CD80, CD83, and CD86 together with MHC class I and II molecules was inhibited. LT ameliorated the attenuation of endocytic capacity during DC maturation by LTA while such effect was not observed in LPS-matured DCs. Furthermore, exposure to LT resulted in a decrease in the expression of pro-inflammatory cytokines including IL-6, TNF-alpha, and IL-12p40 in LTA-stimulated DCs as in LPS-stimulated DCs. Interestingly, LT showed a minimal change in LTA-induced IL-1beta expression while LT highly enhanced the LPS-induced IL-1beta expression. Those inhibitory effects might be associated with LT interference of LTA-signaling pathways mediated through mitogen-activated protein kinases (MAPKs) since LT suppressed phosphorylation of MAPK, which was induced by LTA. Meanwhile, no change was observed in the expression of putative anthrax toxin receptors, TEM8 and CMG2, or Toll-like receptor 2. These results suggest that LT suppresses the maturation and activation of DCs stimulated with LTA, similar to the suppression in the LPS-stimulated DCs, but via a distinct mechanism. |
Databáze: | OpenAIRE |
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