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  • 1
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    Cleavage of fibrinogen by proteinases elicits allergic responses through Toll-like receptor 4 (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-21
    Description: Proteinases and the innate immune receptor Toll-like receptor 4 (TLR4) are essential for expression of allergic inflammation and diseases such as asthma. A mechanism that links these inflammatory mediators is essential for explaining the fundamental basis of allergic disease but has been elusive. Here, we demonstrate that TLR4 is activated by airway proteinase activity to initiate both allergic airway disease and antifungal immunity. These outcomes were induced by proteinase cleavage of the clotting protein fibrinogen, yielding fibrinogen cleavage products that acted as TLR4 ligands on airway epithelial cells and macrophages. Thus, allergic airway inflammation represents an antifungal defensive strategy that is driven by fibrinogen cleavage and TLR4 activation. These findings clarify the molecular basis of allergic disease and suggest new therapeutic strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898200/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millien, Valentine Ongeri -- Lu, Wen -- Shaw, Joanne -- Yuan, Xiaoyi -- Mak, Garbo -- Roberts, Luz -- Song, Li-Zhen -- Knight, J Morgan -- Creighton, Chad J -- Luong, Amber -- Kheradmand, Farrah -- Corry, David B -- AI057696/AI/NIAID NIH HHS/ -- AI070973/AI/NIAID NIH HHS/ -- CA125123/CA/NCI NIH HHS/ -- HL75243/HL/NHLBI NIH HHS/ -- K02 HL075243/HL/NHLBI NIH HHS/ -- R01 AI057696/AI/NIAID NIH HHS/ -- R01 HL095382/HL/NHLBI NIH HHS/ -- R01 HL117181/HL/NHLBI NIH HHS/ -- R25GM56929/GM/NIGMS NIH HHS/ -- T32 GM088129/GM/NIGMS NIH HHS/ -- T32GM088129/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):792-6. doi: 10.1126/science.1240342.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Biology and Molecular Medicine Program, Baylor College of Medicine, Houston, TX, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspergillus niger/growth & development/*immunology ; Aspergillus oryzae/enzymology ; Bronchoalveolar Lavage Fluid/cytology ; Epithelial Cells/immunology/metabolism ; Fibrinogen/*metabolism ; Immunity, Innate ; Ligands ; Macrophage Activation ; Macrophages/immunology/metabolism/microbiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Peptide Hydrolases/immunology/*metabolism ; Respiratory Hypersensitivity/*immunology/*metabolism ; Respiratory Mucosa/cytology/immunology/metabolism ; Th2 Cells/immunology ; Toll-Like Receptor 4/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)
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  • 2
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    Role of Rac1 and oxygen radicals in collagenase-1 expression induced by cell shape change (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Integrin-mediated reorganization of cell shape leads to an altered cellular phenotype. Disruption of the actin cytoskeleton, initiated by binding of soluble antibody to alpha5beta1 integrin, led to increased expression of the collagenase-1 gene in rabbit synovial fibroblasts. Activation of the guanosine triphosphate-binding protein Rac1, which was downstream of the integrin, was necessary for this process, and expression of activated Rac1 was sufficient to increase expression of collagenase-1. Rac1 activation generated reactive oxygen species that were essential for nuclear factor kappa B-dependent transcriptional regulation of interleukin-1alpha, which, in an autocrine manner, induced collagenase-1 gene expression. Remodeling of the extracellular matrix and consequent alterations of integrin-mediated adhesion and cytoarchitecture are central to development, wound healing, inflammation, and malignant disease. The resulting activation of Rac1 may lead to altered gene regulation and alterations in cellular morphogenesis, migration, and invasion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kheradmand, F -- Werner, E -- Tremble, P -- Symons, M -- Werb, Z -- AR20684/AR/NIAMS NIH HHS/ -- DE10306/DE/NIDCR NIH HHS/ -- HL03732/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 May 8;280(5365):898-902.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9572733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Size ; Collagenases/*genetics ; Cytochalasin D/pharmacology ; Enzyme Activation ; Fibroblasts ; Free Radicals ; GTP Phosphohydrolases/genetics/*metabolism ; GTP-Binding Proteins/genetics/*metabolism ; *Gene Expression Regulation, Enzymologic ; Genes, Reporter ; Hydrogen Peroxide ; Interleukin-1/genetics/metabolism ; Matrix Metalloproteinase 1 ; NF-kappa B/metabolism ; Rabbits ; Reactive Oxygen Species/*metabolism ; Receptors, Fibronectin/physiology ; Transcription, Genetic ; rac GTP-Binding Proteins
    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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  • 3
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    Transcellular water transport in lung alveolar epithelium through mercury-sensitive water channels. (1994)
    National Academy of Sciences
    Details
    Publication Date: 1994-05-24
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Ab initio prediction of magnetically dead layers in freestanding γ-Ce(111) (2010)
    American Institute of Physics
    Details
    Publication Date: 2010-10-01
    Print ISSN: 0021-8979
    Electronic ISSN: 1089-7550
    Topics: Physics
    Published by American Institute of Physics
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