Abstract
Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.
MeSH Terms
Antibodies, Monoclonal
Apoptosis
Bacterial Proteins/metabolism,pharmacology
Cell Line/metabolism
Cycloheximide/pharmacology
Cytotoxicity, Immunologic
Drosophila Proteins
Genes, Reporter
Humans
Lipopolysaccharide Receptors/analysis
Lipopolysaccharides/immunology
Lipoproteins/metabolism,pharmacology
Membrane Glycoproteins/immunology,metabolism
Monocytes/cytology,immunology,metabolism
NF-kappa B/metabolism
Protein Synthesis Inhibitors/pharmacology
Reactive Oxygen Species/metabolism
Receptors, Cell Surface/immunology,metabolism
Signal Transduction
Tetradecanoylphorbol Acetate/pharmacology
Toll-Like Receptor 2
Toll-Like Receptors
Transfection
Tumor Cells, Cultured
Chemicals
Antibodies, Monoclonal
Bacterial Proteins
Drosophila Proteins
Lipopolysaccharide Receptors
Lipopolysaccharides
Lipoproteins
Membrane Glycoproteins
NF-kappa B
Protein Synthesis Inhibitors
Reactive Oxygen Species
Receptors, Cell Surface
TLR2 protein, human
Toll-Like Receptor 2
Toll-Like Receptors
Cycloheximide
Tetradecanoylphorbol Acetate
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Aliprantis A O
Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.
Yang R B
Mark M R
Suggett S
Devaux B
Radolf J D
Klimpel G R
Godowski P
Zychlinsky A