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    Prostaglandin D2 as a mediator of allergic asthma (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-17
    Description: Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (TH2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)-mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D2 (PGD2), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP-/-) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of TH2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP-/- mice were greatly reduced compared with those in wild-type animals. Moreover, DP-/- mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD2 functions as a mast cell-derived mediator to trigger asthmatic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, T -- Hirata, M -- Tanaka, H -- Takahashi, Y -- Murata, T -- Kabashima, K -- Sugimoto, Y -- Kobayashi, T -- Ushikubi, F -- Aze, Y -- Eguchi, N -- Urade, Y -- Yoshida, N -- Kimura, K -- Mizoguchi, A -- Honda, Y -- Nagai, H -- Narumiya, S -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2013-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720327" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Asthma/immunology/metabolism/pathology/*physiopathology ; Bronchial Hyperreactivity ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Crosses, Genetic ; Female ; Gene Targeting ; Humans ; Immunoglobulin E/blood ; Interferon-gamma/metabolism ; Interleukins/metabolism ; Lung/immunology/metabolism/pathology ; Lymphocytes/immunology ; Male ; Mast Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mucus/secretion ; Ovalbumin/immunology ; Prostaglandin D2/metabolism/*physiology ; *Receptors, Immunologic ; Receptors, Prostaglandin/genetics/metabolism/*physiology ; Respiratory Mucosa/secretion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Regulation of C. elegans life-span by insulinlike signaling in the nervous system (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-06
    Description: An insulinlike signaling pathway controls Caenorhabditis elegans aging, metabolism, and development. Mutations in the daf-2 insulin receptor-like gene or the downstream age-1 phosphoinositide 3-kinase gene extend adult life-span by two- to threefold. To identify tissues where this pathway regulates aging and metabolism, we restored daf-2 pathway signaling to only neurons, muscle, or intestine. Insulinlike signaling in neurons alone was sufficient to specify wild-type life-span, but muscle or intestinal signaling was not. However, restoring daf-2 pathway signaling to muscle rescued metabolic defects, thus decoupling regulation of life-span and metabolism. These findings point to the nervous system as a central regulator of animal longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolkow, C A -- Kimura, K D -- Lee, M S -- Ruvkun, G -- AG14161/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 6;290(5489):147-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11021802" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*physiology ; Animals ; Caenorhabditis elegans/genetics/*physiology ; *Caenorhabditis elegans Proteins ; Catalase/genetics/metabolism ; Gene Expression Regulation ; Genes, Helminth ; Helminth Proteins/genetics/metabolism ; Intestines/cytology/physiology ; Larva/physiology ; Longevity ; Muscles/cytology/physiology ; Nervous System Physiological Phenomena ; Neurons/*physiology ; Phenotype ; *Phosphatidylinositol 3-Kinases ; Promoter Regions, Genetic ; Receptor, Insulin/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Superoxide Dismutase/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
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