Soluble mediators produced by the crosstalk between microvascular endothelial cells and dengue-infected primary dermal fibroblasts inhibit dengue virus replication and increase leukocyte transmigration
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  • 作者:José Bustos-Arriaga ; Neida K. Mita-Mendoza ; Moises Lopez-Gonzalez…
  • 关键词:Dengue ; Innate immunity ; Skin ; Cellular crosstalk ; Fibroblast and endothelial cells
  • 刊名:Immunologic Research
  • 出版年:2016
  • 出版时间:April 2016
  • 年:2016
  • 卷:64
  • 期:2
  • 页码:392-403
  • 全文大小:1,384 KB
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  • 作者单位:José Bustos-Arriaga (1) (2)
    Neida K. Mita-Mendoza (3)
    Moises Lopez-Gonzalez (1)
    Julio García-Cordero (1)
    Francisco J. Juárez-Delgado (4)
    Gregory D. Gromowski (2)
    René A. Méndez-Cruz (5)
    Rick M. Fairhurst (3)
    Stephen S. Whitehead (2)
    Leticia Cedillo-Barrón (1)

    1. Departmento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados, Instituto Politécnico Nacional, Mexico, Distrito Federal, Mexico
    2. Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
    3. Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA
    4. Departamento de Cirugia, Hospital General Ticomán S.S., Mexico, Distrito Federal, Mexico
    5. Laboratorio de Inmunología UMF, FES Iztacala, Universidad Autónoma de México, Mexico, Distrito Federal, Mexico
  • 刊物主题:Allergology; Immunology; Medicine/Public Health, general; Internal Medicine;
  • 出版者:Springer US
  • ISSN:1559-0755
文摘
When dengue virus (DENV)-infected mosquitoes use their proboscis to probe into human skin during blood feeding, both saliva and virus are released. During this process, cells from the epidermis and dermis layers of the skin, along with small blood vessels, may get exposed to or infected with DENV. In these microenvironments of the skin, the presence of DENV initiates a complex interplay among the DENV-infected and non-infected neighboring cells at the initial bite site. Previous studies suggested that DENV-infected human dermal fibroblasts (HDFs) participate in the immune response against DENV by secreting soluble mediators of innate immunity. In the present study, we investigated whether DENV-infected HDFs activate human dermal microvascular endothelial cells (HDMECs) in co-cultures. Our results suggest that co-cultures of DENV-infected HDFs and HDMECs elicit soluble mediators that are sufficient to reduce viral replication, activate HDMECs, and induce leukocyte migration through HDMEC monolayers. These effects were partly dependent on HDF donor and DENV serotype, which may provide novel insights into the natural variation in host susceptibility to DENV disease.

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