Publikationsdatum:
1999-07-31
Beschreibung:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Antibodies, Monoclonal
;
Antigens, CD14/analysis
;
*Apoptosis
;
Bacterial Proteins/metabolism/*pharmacology
;
Cell Line/metabolism
;
Cycloheximide/pharmacology
;
Cytotoxicity, Immunologic
;
*Drosophila Proteins
;
Genes, Reporter
;
Humans
;
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
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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